844 Matching Annotations
- Jul 2022
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www.lesswrong.com www.lesswrong.com
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The Map Is Not The Territory
- The map is not the territory metaphorically illustrates the differences between belief and reality.
- The phrase was coined by Alfred Korzybski.
Scribbling on the map does not change the territory
- If you change what you believe about an object, that is a change in the pattern of neurons in your brain.
- The real object will not change because of this edit.
The map is a separate object from the territory and the map exists as an object inside the territory
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www.biorxiv.org www.biorxiv.org
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Note: This rebuttal was posted by the corresponding author to Review Commons. Content has not been altered except for formatting.
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Reply to the reviewers
We are sincerely grateful to the reviewers for several key comments that led us to correct some mistakes and better appreciate how to put our findings in the context of recently published data. These changes undoubtedly improved the manuscript.
Many other reviewer comments seem to equate chaperone binding with a functional chaperone role in de novo folding. These are not the same. Cytosolic chaperones presumably “sample” nearly every protein that is synthesized by cytoplasmic ribosomes. This does not mean that every such protein would misfold if even one of those chaperones failed to bind it. If we want to understand what chaperone mutations might cause human disease due to septin misfolding, for example, it will not be enough to catalog all the chaperones that bind septins. We have already done that. What will help is to understand which chaperones make functional contributions to septin folding and complex assembly. Our study is the first to experimentally address chaperone roles in de novo septin folding, period. We take responsibility for not being sufficiently clear about the goals of our work, and, to emphasize these points, we added one sentence to the Introduction and revised another.
Another consistent criticism was that the use of the E. coli system, both in vivo and in vitro, limited our ability to gain insight into the folding of septins in eukaryotic cells and led to a “tessellated view”. For example, reviewers claimed that our model about translation elongation rates for Cdc12 were “based mainly on the E. coli system and bioinformatics analysis”. We disagree with this interpretation. Key evidence in support of our model come from published data in yeast, specifically the much higher density of ribosomes on Cdc12 and the accumulation of ribosomes on the Pro-rich cluster near the Cdc12 N terminus. These are precisely the kinds of “more stringent analysis” in “authentic yeast” (to use Reviewers’ language) that we would have wanted to do to test our model, had they not already been done by others. Without specific suggestions, we struggle to imagine what other kinds of experiments the Reviewers have in mind, apart from a eukaryotic version of a reconstituted cell-free translation system, which Reviewer #1 admits “would be substantially difficult” and “time consuming”. While we are intrigued by the reconstituted eukaryotic cell-free translation system that was published last year (which we mentioned on lines 994-995) and look forward to exploring it in future studies, it is not commercially available and we agree that the amount of effort required to prepare it ourselves is unrealistic for the current study. Most importantly, we do not find in the critiques provided any specific reason why our E. coli-based systems experiments are intrinsically less “stringent” or “rigorous”.
Accordingly, we think that, together with the results of multiple new experiments (detailed below), the extensive re-writing and re-ordering that we have done in the revised manuscript will be enough to better emphasize the importance and rigor of our findings and thus to address all of the Reviewers’ specific concerns.
Reviewer 1 thought that our manuscript “does not even provide new information, since the involvement of CCT and the Hsp70 system is not novel” and thought that “the key finding of this manuscript is how chaperones are involved in the de novo folding of septins, which is not conceptually new because of previous findings, including those of the authors”. Reviewer #3 also stated that “the function of Tric/CCT in septin folding and assembly is well documented”.
We were quite surprised at this reaction, since we dedicated a significant portion of the original manuscript (lines 68-76 and 319-322) to explicitly discussing the only other paper in the literature that specifically addresses the question of whether or not CCT is required for de novo septin folding. As a reminder, that paper explicitly stated that “it is unlikely that CCT is required to fold septins de novo” and “septins probably do not need CCT for biogenesis or folding”. With regard to involvement of the Hsp70 system, the only existing evidence in the literature on this subject is the aggregation of some septins in ssb1∆ ssb2∆ cells. Like the CCT study, that study did not distinguish whether this was a result of problems during septin synthesis and before septin complex assembly, or, alternatively, whether pre-folded and assembled septins were subject to disassembly, misfolding, and aggregation. Our experiments specifically test the fate of newly-synthesized septins prior to assembly in living cells. Our previous findings documented physical interactions between wild-type septins and multiple chaperones but did not address whether these interactions had any functional relevance. We previously reported functional effects of interactions between chaperones and MUTANT septins but, again, these studies did not address functional chaperone requirements for WILD-TYPE septins. While we did our best to highlight these points in the original document without devoting excessive amounts of text, we accept responsibility for not making these points sufficiently clear and to address this issue we added additional text, including the text quoted above, to the Introduction.
While Reviewer #3 commented that the manuscript “is overall well presented”, Reviewer 1 thought that the manuscript was “complicated to read” with “no logical connections, just a list of many results” and mentioned that part of the difficulty was “that it contains many negative results”.
In addition to reorganizing the manuscript, as suggested by the reviewers, we added more text at the beginning and end of nearly every section to even more explicitly state the logical connections between results. In our opinion, negative results of properly controlled experiments are valuable to the research community, and we do not understand what it is about negative results that makes them difficult to read about. Many of the extra experiments we performed were in anticipation of being asked to perform them by reviewers, some of which generated negative results. We are reluctant to remove negative results unless there is a more compelling reason. For example, to address another reviewer concern, we did remove the negative results with the Ydj1–Ssa2 compensatory mutants.
Reviewer #2: “4) Figure 2: The labeling on the protein structure makes it seem like the exact region for Ydj1 and Hsp70 was experimentally identified, when it hasn’t.”
We acknowledge that the first sentence of the figure legend (“the colored ribbon follows the color scheme in the sequences at right for overlapping β-aggregation, Ydj1 and Hsp70-binding sites”) could be misinterpreted, since only in the second sentence does it say “Sequence alignments show predicted binding sites”. We corrected this mistake, and added the text “Predicted chaperone binding sites” as the first words in the legend to this figure.
Reviewer #2: “8) The authors confusingly jump back and forth between different Septins and different chaperone (Ssa1-4, Ydj1, Sis1, Hsp104). We would ask the authors to re-arrange the manuscript, collating all the yeast work in one section and bacterial work in another.”
We re-arranged the manuscript and put all the yeast work in one section and all the bacterial work in another, with the exception of the studies of individually purified Cdc3 and Cdc12, which we put in between the yeast studies of the kinetics of de novo assembly and the yeast studies of post-translational assembly. Our reasoning is that the studies with the purified proteins demonstrate challenges with maintaining native conformations in the absence of chaperones and other septins, which flows naturally into the yeast studies asking about the ability of “excess” septins to maintain oligomerization-competent conformations in the absence of other septins and when we experimentally eliminate specific chaperones. All of the work actually manipulating E. coli genes/proteins is now together.
Reviewer #3: “1. The co-translational binding of CCT to nascent polypeptide chains has been studied (Stein et al., Mol Cell 2019). While the authors indicate that septin subunits are engaged co-translationally, they do not comment which ones are interacting with CCT and at which state of translation. This information is crucial and should also be mentioned in the discussion section.”
We are grateful to the Reviewer for bringing up this point, which we had overlooked. We hadn’t noticed that, in the end, only Cdc3 met the CCT confidence threshold to be included in the supplemental data of the Stein et al. paper. All septins co-purified with CCT in an earlier Dekker et al proteomic study, so we strongly suspect that the failure of the other septins to meet the confidence threshold in the Stein et al paper reflects the sensitivity of that assay, rather than a significant difference in how septin GTPase domains interact with CCT. We also hadn’t appreciated that according to that study, the main sites in the Cdc3 GTPase domain bound by CCT and Ssb are the same. Hence our statement that Ssb bound to septins “earlier” during translation, and CCT bound “later” was wrong. Instead, the overlapping Ssb and CCT site in Cdc3 turns out to be remarkably consistent with a conclusion from Stein et al paper, that CCT binds Rossmann-fold proteins like septins at sites where “early” beta strands have been translated and expose a chaperone-binding surface that later becomes buried by an alpha helix. We corrected our mistake in the text and in our model figure and added: (1) a new supplemental figure with predicted septin structures and a sequence alignment indicating where CCT and Ssb bound; and (2) text discussing the confidence thresholds for “calling” septin-CCT interaction, the Rossmann-fold binding, and how we interpret Ssb and CCT binding to the same site.
Reviewer #3 “3. Figure 3: It is recommended to also follow Cdc10-GFP and Cdc12-GFP fluorescence. This will on the one hand generalize the presented findings and provide a direct link to other parts of the study (e.g. crosslinking analysis of Cdc10).
We carried out the requested experiment for Cdc12, using Cdc12-mCherry rather than Cdc12-GFP because of the formation of non-native foci that we observed with Cdc12-GFP. We also attempted to analyze Cdc10, using an existing GAL1/10-promoter-driven Cdc10-mCherry plasmid that we’d made a few years ago, but it did not behave as expected, with high expression even in the absence of galactose (not shown), which prevented us from performing the requested experiment. We have a Cdc10-GFP plasmid with the inducible MET15 promoter, but this promoter does not provide sufficiently low levels of expression in repressive conditions, so there would be too much expression at the beginning of the experiment for us to accurately follow accumulation thereafter. Instead, we tried the only other plasmid we had with the GAL1/10-promoter controlling a tagged septin: Cdc11-GFP. Above a certain threshold of expression, Cdc11-GFP formed unexpected cortical foci, but we were still able to perform the analysis and found a clear delay in septin ring signal in cct4 cells, providing the requested generalization to other septins, if not Cdc10.
Reviewer #3 “5. Figure 4C: The finding that only ssb1 but not ssb2 knockouts have an effect on joining of free Cdc12-mCherry subunits into septin rings is puzzling. Similarly, Ssb1 largely acts co-translationally, while in this assay post-translational septin ring assembly is monitored. The authors need to comment on these two points.”
We did not examine ssb2 knockouts, so we do not know to what the Reviewer is referring in the first point. If the Reviewer means that they are puzzled by the fact that we saw a phenotype in cells in which only SSB1 was deleted and SSB2 remained, we offer two explanations. As can be seen in the Saccharomyces Genome Database entry for SSB1 (https://yeastgenome.org/locus/S000002388/phenotype), there are at least a dozen known phenotypes associated with deletion of SSB1 in cells with wild-type SSB2. We even showed a very clear septin misfolding/mislocalization phenotype in Supplemental Figure 4D. Thus while our findings are new and provide novel insights into Ssb function, they are not unprecedented. The Reviewer is correct that most Ssb is ribosome-bound and thus Ssb1 “largely acts co-translationally” but ~25% of Ssb is not ribosome-associated (PMID: 1394434). Furthermore, the lack of a strong phenotype for ssb1∆ cells in our new kinetics-of-folding experiment (see below), plus the realization that Ssb and CCT both bind the same site in Cdc3, leads us to a new model: Ssb acts both co- and post-translationally in septin folding, but only the post-translational function is associated with a phenotype in ssb1∆ cells, because in that assay we drastically overexpress a tagged septin and thereby exceed the Ssb chaperone capacity that remains when we delete SSB1. This logic also explains the first ssb1∆ phenotype we saw, when overexpressing Cdc10(D182N)-GFP. In the kinetics-of-folding assay, on the other hand, tagged septin expression is much lower and reducing the amount of total Ssb by ~50% (via SSB1 deletion) likely does not compromise Ssb function in folding the tagged septin. We therefore removed our statement that “Ssb dysfunction leaves nascent septins in non-native conformations that are aggregation-prone and unrecognizable to CCT”, revised our model figure accordingly, and added new text and citations to explain our new model.
Reviewer #3 “Additionally, they should test whether the appearance of septin ring fluorescence is slowed down in ssb1 mutants (as shown for cct4-1 mutant cells in Figure 3B).”
We agree that slower septin folding in ssb1∆ cells is a prediction of our model, and we performed the requested experiment and include the results in our revised manuscript. The new data show that the appearance of septin ring fluorescence is not delayed in ssb1∆ mutants, which is easily explained by the ability of Ssb2 to chaperone the folding of the low levels of tagged septin that we express in these kinds of experiments (see above).
Reviewer #3: “7. Figure 5G: The data is not convincing. This reviewer cannot detect a specific Cdc12 band accumulating in presence of GroEL/ES.”
We re-ran the reactions again with fresh reagents and this time ran the gel longer to reduce excess signal from free fluorescent puromycin and the bright Cdc10 bands. We now see a very clear band for full-length Cdc12 in the reaction with added GroEL/ES, fully consistent with our mass spectrometry results. We updated the figure with the new results.
Reviewer #3: “Furthermore, the activity tests done for the chaperonin system are confusing (Supplemental Figure 7). The ATPase rate (slope!) of GroEL/GroES seems higher as compared to GroEL but according to the authors it should be opposite.”
In our assays, the ATPase activity is so fast that for our “time 0” timepoint, much of it has already occurred by the time the reaction can be physically stopped and measured. In other words, the handling time is such that we can’t visualize what happened in the earliest stages of the reaction, where the rates could accurately be estimated as slopes. This is obvious from the fact that at time 0, the absorbance for the “GroEL alone” reaction is already more than twice the absorbance for GroEL+ES. We added clarifying text to the figure legend.
Reviewer #3: “The refolding assay using Rhodanese as substrate is also confusing: What is the activity of native Rhodanese? The aggregated Rhodanese sample seems to have substantial activity that is not too different from a GroEL/ES-treated one. From the presented data it is not clear to the reviewer to which extend GroEL/ES prevents aggregation and supports folding of denatured Rhodanese.”
We thank the Reviewer for bringing this to our attention, because made we mistakenly left out the values for native Rhodanese with the reporter. With regard to the aggregated Rhodanese, we failed to note that this sample contains urea. When the urea absorbance is subtracted, it is clear that the GroEL/ES-treated sample has higher activity. Furthermore, some native enzyme is likely still active within the aggregated sample, explaining the “substantial activity” that the Reviewer correctly notes. We corrected the figure and added clarifying text to the figure legend.
Reviewer #3: “the study goes astray following aspects that does not seem relevant to this reviewer (e.g. the role of N-terminal proline residues for Cdc12 translation, Fig. 5E/F).”
We acknowledge that we did a poor job of introducing the N-terminal Pro-rich cluster in Cdc12 with relation to our model of slow Cdc12 translation. Instead, we have revised and reorganized the manuscript to set up these experiments as a direct test of our model: if ribosome collisions on the body of the ORF drive mRNA decay, then decreasing the spacing of those ribosomes should exacerbate the problem, and eliminating the Pro-rich cluster (where published yeast data already show ribosomes accumulate) is the most logical way to test the prediction. Far from being irrelevant, the results fit the prediction perfectly and thus support the model. We expect that this change will highlight the importance of these experiments for the reader.
Reviewer #2: “1) Fig. 1 Is the folding of Cdc3 being measured in cells lacking chaperones mentioned towards the end of the paper or are the authors referring to the lack of yeast proteins?”
We are unclear as to what the Reviewer is asking here. The title of Figure 1 states that these are “purified yeast septins” and the figure legend further emphasizes this fact. Additionally, the Coomassie-stained gel in Figure 1A shows a single band, corresponding to purified 6xHis-Cdc3. The proteins were purified from wild-type E. coli cells, so all E. coli chaperones were present when Cdc3 initially folded, but chaperones and all other proteins were removed during the purification and prior to the analysis. We do not know what change to make.
Reviewer #2 asked “How do the authors account for the septin defect in Ssa4 delete cells in unstressed conditions where Ssa4 would be very low already? According to the authors previous work, Ssa2 and 3 should be able to compensate.”
We explicitly addressed this point in the original manuscript (lines 893-898). Again, we think here the Reviewer is equating chaperone binding with chaperone function. According to our previous work, Ssa2 and Ssa3 are able to bind septins, but this does not mean that they can fold septins the same way as Ssa4. We cite several papers that discuss the distinct functional roles for the different Ssa proteins. We do not think that additional clarification of this point would strengthen the manuscript.
Reviewer #3: “6. Figure 5B: It is unclear why Cdc3 is observed in the pulldown of His-tagged Cdc12 (37˚C), although no Cdc12 was isolated under these conditions. How is that possible?”
That is not possible. As we indicate in the figure legend and with the red asterisk, the only band appearing in that lane is a non-specific band that cross-reacts with the anti-Cdc3 and/or anti-Cdc11 antibodies. This is why it is also present in the “No septins” control lanes. We made the asterisk larger to help accentuate this point.
Reviewer #3: “Furthermore, the authors observe a specific effect on Cdc12-Cdc11 assembly in the E. coli groEL mutant. How do they rationalize this specific effect as Cdc12-Cdc3 assembly remained unchanged? This observation also seems in conflict with the suggestion of the authors that Cdc12 preferentially recruits Cdc11 before interacting with Cdc3 (page 45, lane 1024).”
Cdc11 was not expressed in the groEL mutants because no Cdc11 gene was present in those cells, as explained in the body text and indicated in the labeling above the lanes in Figure 5A. The band near the size of Cdc11 is a non-septin protein that bound to the beads in the groEL-mutant cells, as is shown in the immunoblot using anti-Cdc11 antibodies in Figure 5B. Thus there is no conflict to rationalize.
Reviewer #1: “The only evidence that CCT binds to septin is the list of LC-MS/MS. Western blotting would provide more solid data.” and “2) The cross-linking experiments appears not to have been successful. Why are the Ssas, Ydjs etc not detected here? “
First, CCT subunits are relatively low-abundance, expressed at 5- to 50-fold lower levels than other chaperone families in the yeast cytosol (see PMID: 23420633). To the Reviewer’s second point, we did in fact detect other chaperones in our crosslinking mass spectrometry experiments, including Ydj1, multiple Ssa and Ssb chaperones, Hsp104, etc., as can be seen in Table S1. However, they were also detected in negative control experiments. This is not surprising, given that these chaperones are among the most common “contaminants” of affinity-based purification schemes (see the CRAPome database at https://reprint-apms.org/). It was for this reason we had to perform so many negative control experiments, which likely produced some false negative results, as some “real” interactions were likely discarded when the same chaperone showed up in our controls. We added a figure panel with a Venn diagram of overlap between experimental and control samples, and text pointing out this caveat of our approach.
Second, in this experiment we attempted to identify proteins that transiently interact with a specific region of Cdc10 that will later become buried in a septin-septin oligomerization interface. Due to the transient nature of the interaction, we do not expect to detect high levels of crosslinked chaperones. Mass spectrometry is significantly more sensitive than immunoblotting, so there is no guarantee that we would be able to detect a band even if the crosslinking works as desired. Indeed, the crosslinked bands we saw by immunoblot for GroEL were quite faint (see Figure 2F), despite the fact that GroEL and the T7-promoter-driven Cdc10 were among the most abundant proteins in those E. coli cells.
Third, there is no commercially available, verified antibody recognizing yeast Cct3 for which to perform the requested immunoblot experiment. Since both the N and C termini of CCT subunits project into the folding chamber, it is unwise to use a standard epitope tagging approach, as the tags may compromise function. Indeed, for purification purposes others inserted an affinity tag in an internal loop in Cct3 (PMID: 16762366). We have a yeast strain with Cct6 tagged in an analogous way, but to perform the requested immunoblot experiment with Cct3 would require creating or obtaining the Cct3-tagged strain, deleting NAM1/UPF1, and introducing our Bpa tRNA/synthetase and GST-6xHis-Cdc10 plasmids. Given the sensitivity of detection concerns stated above, we doubt this would help.
In summary, we prefer not to attempt the requested immunoblot experiments.
Reviewer #1: “-Fig. 3B ant related Figures: The experiment to see if GFP-tagged septin accumulates in the bud neck is important, but only the graphs after the analysis are shown. The authors should provide the readers with representative examples from imaging data.”
We are confused, because the images at the bottom of Figure 3A already show what the Reviewer requests. As stated in the figure legend, these are representative examples of the imaging data from a middle timepoint of one of the experiments. It would be nearly impossible (for space reasons) to provide representative images for all of the timepoints for all of the genotypes for all of the experiments. Since in our new experiments we introduce new tagged septins (Cdc11-GFP and Cdc12-mCherry), we also now include representative images of cells expressing these proteins, as well.
Reviewer #2: “3) If the authors had evidence of chaperone interaction from their previous study, why did they not simply do IPs with fragments of the septins/chaperones?”
We are unclear why the Reviewer is suggesting IPs after referring to our previous study. IPs are a poor choice for transient interactions, which is why we mostly avoided them in previous studies, and instead used a novel approach (BiFC) to “trap” chaperone–septin interactions. Moreover, we seek to identify chaperones that bind wild-type septins at future septin-septin interfaces on the path towards the native conformation. Fragments of septin proteins would likely misfold and would therefore likely attract chaperones that wouldn’t normally bind the full-length septin. Indeed, our previous studies demonstrated that even a single non-conservative amino acid substitution was sufficient to alter chaperone-septin binding. Thus IPs with fragments of septins or chaperones would be highly unlikely to yield informative results for the questions we seek to answer. We strongly prefer not to attempt these suggested experiments.
Reviewer #2: “5) While differences between Ssa paralogs are highly interesting, using deletions of Ssas is not useful, given that yeast compensate by overexpressing other paralogs. The yeast GFP Septin assays should be repeated in yeast lacking all Ssas and expressing one paralog on a constitutive promoter (See numerous papers by Sharma and Masison).”
We disagree that ssa deletions are “not useful”, since if the overexpressed paralogs cannot fulfill the same function as the deleted SSA, then we will see a phenotype. Which we do. Furthermore, we had already obtained and thoroughly tested a strain like the ones mentioned by the reviewer (ECY487, a.k.a. JN516, from Betty Craig’s lab, with ssa2∆ ssa3∆ ssa4∆ and SSA1, which is constitutively expressed, PMID: 8754838), but we found that, as published, it divides slightly more slowly even under the most permissive of conditions. The requested strain cannot be analyzed using our method, because slow accumulation of ring fluorescence could be attributed to other defects unrelated to septin folding. Thus we strongly prefer not to attempt the suggested experiments.
Reviewer #2: “7) The authors need to clarify the experiment with the Ydj1 D36N and Ssa2 R169H. In Reidy et al, they never fully biochemically test this system and it was never examined for Ssa2-Ydj1. The authors would need to do some fundamental experiments to demonstrate the validity and functionality of this double mutant in yeast.”
Given that this experiment was unable to generate meaningful data, since the mutations affected the kinetics of induction of the GAL1/10 promoter, we do not think the requested biochemical experiments would add any value to the study. Instead, we removed these studies from the manuscript.
Reviewer #3: “4. Figure 3B: The difference between wt and cct4-1 cells in appearance of septin ring fluorescence is observed at one timepoint. Since this experiment is considered highly relevant, the authors are asked to include another timepoint to bolster the conclusion that Cdc3-GFP folding and thus septin ring assembly is delayed in the CCT mutant.”
We carried out new experiments with cct4-1 cells using Cdc12-mCherry and Cdc11-GFP with more timepoints than in our original cct4-1 experiments with Cdc3-GFP. Since these experiments provide the same kinds of results, but at multiple timepoints, we do not see the value in repeating the Cdc3-GFP experiment.
Reviewer #3: “If Ssb1 functions to maintain Cdc12 in an assembly competent state preventing misfolding, one would expect either enhanced degradation or aggregation of Cdc12-mCherry in ssb1 mutant cells. Did the authors check for such scenario? Septin aggregation has been shown in a ssb1 ssb2 double deletion strain (Willmund et al., 2013), yet the data shown here predict that aggregation might already occur in single ssb1 mutants.”
We already examined septin aggregation in single ssb1 mutants and showed these data (Supplementary Figure 4D). Indeed, this phenotype was the rationale for testing post-translational septin assembly in ssb1 single mutants. We have seen no evidence of septin degradation in any context (as we mentioned on line 889), so we would not expect it here. While we added new text and a very new citation showing that many “misfolded” conformations of wild-type E. coli proteins avoid aggregation and degradation, we do not think that the suggested experiments would add enough value to the current study to justify the effort, time and expense.
Reviewer #3: “Fig. 3C: The figure showing septin ring fluorescence does not include error bars. This is crucial, also because the difference between wt and ssa4 mutant cells is not large.”
There are, in fact, error bars included in the figure, as can be most clearly seen for the final timepoint for the ssa4∆ cells. For most of the other timepoints the error bars are smaller than the data point symbols (the circles and squares). We do not think that adjusting the size or opacity of the symbols to better show the error bars will be sufficiently valuable to justify the effort.
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www.zylstra.org www.zylstra.org
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https://www.zylstra.org/blog/2022/06/spring-83/
I've been thinking about this sort of thing off and on myself.
I too almost immediately thought of Fraidyc.at and its nudge at shifting the importance of content based on time and recency. I'd love to have a social reader with additional affordances for both this time shifting and Ton's idea of reading based on social distance.
I'm struck by the seemingly related idea of @peterhagen's LindyLearn platform and annotations: https://annotations.lindylearn.io/new/ which focuses on taking some of the longer term interesting ideas as the basis for browsing and chewing on. Though even here, one needs some of the odd, the cutting edge, and the avant garde in their balanced internet diet. Would Spring '83 provide some of this?
I'm also struck by some similarities this has with the idea of Derek Siver's /now page movement. I see some updating regularly while others have let it slip by the wayside. Still the "board" of users exists, though one must click through a sea of mostly smiling and welcoming faces to get to it the individual pieces of content. (The smiling faces are more inviting and personal than the cacophony of yelling and chaos I see in models for Spring '83.) This reminds me of Stanley Meyers' frequent assertion that he attempted to design a certain "sense of quiet" into the early television show Dragnet to balance the seeming loudness of the everyday as well as the noise of other contemporaneous television programming.
The form reminds me a bit of the signature pages of one's high school year book. But here, instead of the goal being timeless scribbles, one has the opportunity to change the message over time. Does the potential commercialization of the form (you know it will happen in a VC world crazed with surveillance capitalism) follow the same trajectory of the old college paper facebook? Next up, Yearbook.com!
Beyond the thing as a standard, I wondered what the actual form of Spring '83 adds to a broader conversation? What does it add to the diversity of voices that we don't already see in other spaces. How might it be abused? Would people come back to it regularly? What might be its emergent properties?
It definitely seems quirky and fun in and old school web sort of way, but it also stresses me out looking at the zany busyness of some of the examples of magazine stands. The general form reminds me of the bargain bins at book stores which have the promise of finding valuable hidden gems and at an excellent price, but often the ideas and quality of what I find usually isn't worth the discounted price and the return on investment is rarely worth the effort. How might this get beyond these forms?
It also brings up the idea of what other online forms we may have had with this same sort of raw experimentation? How might the internet have looked if there had been a bigger rise of the wiki before that of the blog? What would the world be like if Webmention had existed before social media rose to prominence? Did we somehow miss some interesting digital animals because the web rose so quickly to prominence without more early experimentation before its "Cambrian explosion"?
I've been thinking about distilled note taking forms recently and what a network of atomic ideas on index cards look like and what emerges from them. What if the standard were digital index cards that linked and cross linked to each other, particularly in a world without adherence to time based orders and streams? What does a new story look like if I can pull out a card either at random or based on a single topic and only see it or perhaps some short linked chain of ideas (mine or others) which come along with it? Does the choice of a random "Markov monkey" change my thinking or perspective? What comes out of this jar of Pandora? Is it just a new form of cadavre exquis?
This standard has been out for a bit and presumably folks are experimenting with it. What do the early results look like? How are they using it? Do they like it? Does it need more scale? What do small changes make to the overall form?
For more on these related ideas, see: https://hypothes.is/search?q=tag%3A%22spring+%2783%22
Tags
- Pandora's box
- quiet
- atomic idea links
- combinatorial creativity
- Fraidyc.at
- yearbooks
- Now Now Now
- Markov monkey
- narrative forms
- Dragnet
- read
- cadavre exquis
- Derek Sivers
- atomic notes
- Spring '83
- experimental fiction
- index cards
- Lindy library
- media studies
- calmness
- web standards
- experimental media
- alternate universes
Annotators
URL
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- Jun 2022
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doubleloop.net doubleloop.net
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h0p3 has a home page entry point that is carefully curated and groomed, but which is several layers up from a complete chaos of link dumps, raw drafts and random introspections […] These layers run a spectrum of accessibility—there is always a learning curve before you hit the bottom. You start with a doorway before entering a maze.
carefully cureated groomed
chaos of link dumps
you start with a door way before entering a maze
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As Kick’s wrote (https://www.kickscondor.com/stenos/we've-got-blog/):
wow
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Also learned about are.na, which says it provides ‘tools for thinking, together‘. Which I like the sound of, but as are.na is a silo, it’s not something I will be using personally.
!- pearl : tools for thinking, together
https://doubleloop.net/wp-content/uploads/2020/11/doubleloop.png
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www.biorxiv.org www.biorxiv.org
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Note: This rebuttal was posted by the corresponding author to Review Commons. Content has not been altered except for formatting.
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Reviewer #1 (Evidence, reproducibility and clarity (Required)): **Summary:** Techniques to probe the local environment of membrane proteins are sparse, although the influence of lipids on the membrane protein's function are known since many years. Therefore, the paper by Umebayashi et al. is important. The environment-sensitive dye Nile red (NR) coupled to a membrane protein is an appropriate sensor for monitoring the local membrane fluidity. Linking of Nile red to the receptor via a flexible tether was achieved with the acyl carrier protein (ACP)-tag method. Experiments showed that depending on the ACP site a certain linker length is required to have NR inserted in the membrane and thus be an effective sensor for lipid disorder. This technology could be of general usability to study the environment of membrane proteins in the context of their function. As an example, the technique allowed insulin induced membrane disorder in the close insulin receptor vicinity to be observed. Further, results suggested that tyrosine activity is required for this disorder to happen. The experimental results appear to be complete and controls were made.
**Major comments:** 1) Sometimes technical terms are used without explanation: What is the GP value? What is ACP-IR? The spectrum was measured in number of rois? The reader can find those abbreveations out, but it would be nice to have them defined.
We have made a list of abbreviations.
2) Fig. 1d) is confusing. The ACP-IR labelling is evident in 3 panels, but there is no difference in the color (emission spectra of 1992-ACP-IR vs 2031-ACP-IR should be visible??). The DAPI staining is very different. When doing the latter, how difficult is it to get the staining equal?
The differences in spectra cannot be seen because we used pseudo colors for display of the DAPI and CoA-PEG-NR staining. The reviewer’s comments about the unequal DAPI staining is correct. The reason for this is most likely that the cell membrane is unequally permeabilized by PFA treatment. As the point of this figure is just to show that the plasma membrane is labeled, dependent upon the expression of the ACP-tagged insulin receptor, we don’t think that the variable intensities of the DAPI staining is important. DAPI is simply used to indicate the position of the cells.
3) How can one interpret Fig. 4: a) Control goes over 4 frames, at 240" insulin is added, and 10 frames should show a fluctuation difference?
We showed 4 frames after control treatment that showed no significant change was observed by control treatment. We expected that clear changes would be invoked by insulin treatment in GP images, however these changes, while visible in the GP images, are difficult to see for the untrained observer. This is the reason why we used the ZNCC method in the subsequent figures to better visualize the changes.
- b) A color shift from blue to green is visible after insulin addition. But it is faint - difficult to assess from the pseudo color scheme. What does 1000 pixel top/1000 pixel bottom mean in c). Is it an attempt to better visualize the fluctuation? It is difficult to recognize a difference before and after adding insulin. d) It seems that the kymograph set should show this. What is the color scale? Why is 3 so untypical, i.e., no change? Box 6 is also peculiar: the left side does not show a strong change upon insulin administration, the right side does. Why? We appreciate the helpful comments for improving our manuscript.
As pointed out, the change of GP value is extremely small before and after insulin addition, so it is difficult to fully visualize the change with normal pseudo-color expression. To deal with this, we adopted the following two methods to visualize minute changes.
1) Visualization of local changes of the statistical GP value showed by ZNCC throughout the time-lapse images (Fig. 6 and Fig. S2B).
2) Visualization of the top/bottom 1000 pixels of the sorting ZNCC value in each image (Fig. 7 and Fig. S2C). The top 1000 pixels are the ones that showed the largest changes. The bottom 1000 pixels are the ones that showed the smallest changes.
Owing to these expressions, we found out that the level of the response against the insulin signal was spatially and temporally heterogeneous in the membrane.
As for the color scale, in order to clarify the meaning of the difference of color, we have added the description about the relationship between the color and the ZNCC value in the results section.
4) How is the kymogram calculated? The legend says 'The horizontal dimension represents the averaged ZNCC inside the rectangular area, and the vertical dimension represents time'. The averaged ZNCC is a single value, so it is not clear why the kymogram shows a variation from left to right. May it be the ZNCC was averaged just vertically?
We apologize that we did not provide information regarding making the kymograph.
In the yellow rectangular area (Fig. 6B), the ZNCC values of the pixels with the same x coordinate value were vertically averaged, which were represented as the horizontal direction of the kymograph. That is, one horizontal line of the kymograph holds the spatial distribution of the ZNCC value along the horizontal direction of the membrane, and the vertical direction shows their time changes. To make it easier to understand, we refined the description about the kymograph in the legend of Fig. 6.
5) When calculating cross-correlation values on images, they need to be aligned. What fraction of the total image does the selected 19x19 box represent? As described, I imagine that a rolling CC over 19x19 pixels is calculated over an image from the time lapse series comparing it with the reference Iave(x,y). Compared to the 3x3 median filtered CP image, the ZNCC image should then be much more blurred??
Below we provide more information regarding the calculation of ZNCC.
Each local window for ZNCC calculation is set to a 19x19 pixels centered on every single pixel excluding the edges of an image. The ZNCC value calculated in that window is set to a center pixel of that area. After that, a new window centered on the adjacent pixel is set and calculate the new ZNCC. That is, the calculation window is slid throughout the image. Also, the calculated ZNCC value is not set to all the pixels of the window, but is set to only the center pixel of the window, so there is no blur effect like median filtering.
The figure below shows a schematic view of our ZNCC calculation.
Schematic view of our ZNCC calculation
**Minor comment:** On page 16 supplementary is not spelled properly.
corrected
Reviewer #1 (Significance (Required)):
The key point of this paper is convincing and the new technology appears to have a lot of potential. It can be applied to study membrane protein function in the context of its environment, the lipid bilayer.
Membrane fluidity measurements have been developed (e.g., using fluorescent probes like laurdan). However, the trick to link a probe like nile red by ACP technology to the insulin receptor and to observe its activity is quite new.
A most recent description of such a technology is in TrAC Trends in Analytical Chemistry Volume 133, December 2020, 116092.
This is an interesting review, but not directly impacting on our work.
**Referees cross-commenting**
All comments are constructive and important. The paper is important but needs to be amended as proposed.
Reviewer #2 (Evidence, reproducibility and clarity (Required)): **Summary:** In this manuscript, authors generated an ACP-attached Nile Red probe in order to specifically label Insulin receptor in the membrane. Owing to this specificity, one can measure the lipid membrane properties around a specific protein in the membrane. **Major comments:**
For the conclusions in the manuscript to be convincing, in my opinion, these additional data need to be added. Some of these are new experiments, and some are detailed analysis of existing data. The new experiments are not for new line of investigation, instead it is to confirm their statements and conclusions. The major point is the reliability of spectral shift. In usual environment sensitive probes, it is certain that they are in the membrane whatever is done to the membrane. However, when the probe is attached to a protein, it is not trivial to have the same confidence that the probe is always inside the membrane, and it is in the same plane of the membrane. 1992-ACP-IR is a good example; authors state that it binds to the protein outside the membrane, but when there is cholesterol addition and -maybe more interestingly- cholesterol removal, the dye still reacts and changes its emission (even PreCT changes its emission quite a bit at the 570 nm region). This is a clear indication of a change in localization of the probe upon some changes in the membrane. This implies that observed spectral shifts may not be due to lipid packing differences, but due to localization of the probes. For this reason, it is crucial to know where any environment sensitive probe localize in the membrane with respect to membrane normal, and this knowledge is more important for this probe. Related to this, the spectral difference upon insulin treatment and activation of insulin receptor could be due to changes in probe's localization in the membrane. Especially because authors show in Fig1e, the spectra can change depending on the probe localization. Relatedly, quantum yield of NR should be significantly different when it is inside vs outside membrane. Authors should show QY for 1992-ACP-NR and 2031-ACP-NR with different PEG lengths and upon insulin treatment.
We understand the logic of the request to measure the QY, since the QY of Nile red is much higher in organic solvents than in aqueous solutions, so it might be predicted that the QY of Nile red is higher in a lipid bilayer than when covalently bound to the protein in an aqueous environment. However, this argument depends upon the mechanism for the increase in quantum yield when going from aqueous to a non-polar solution. One possible explanation is based on the intrinsic properties of the dye under the two conditions. The alternative explanation would be that the dye would aggregate (be insoluble) in aqueous solution and therefore either not fluoresce or self-quench. In this case, we believe that the latter is the explanation because we and others have previously shown the turn-on properties of the probe when binding to proteins (SNAP-tag and others). It is not simple to measure QY in the cell under a microscope, but we have done something similar shown in supplementary figure 4. We labeled the three ACP-receptor complexes with PEG11-Nile red and co-stained with antibody to the Insulin Receptor. We then calculated a relative quantum yield. There were very little differences at all between the relative quantum yields, so we conclude that it is not the environment of the probe, which affects the quantum yield under these conditions, but the fact that it is covalently attached to a protein and incapable of forming aggregates. What distinguishes these constructs is the emission spectrum, not the quantum yield. In supplementary Table 2 we also did QY measurements in vitro and we could reproduce the increase of quantum yield by association with liposomes or in organic solvents. We tested whether non-covalent association with a protein would increase the QY by incubation with the lipid binding protein, BSA, in PBS. This was not the case, strongly pointing to the conclusion that it is the covalent association with the protein that increases the QY, not association with a protein. We believe that our demonstration of changes in fluorescent spectra with changes in cholesterol, large changes in fluorescent spectra with linker length for the 1992 construct and voltage sensitivity using patch-clamp prove that the Nile red is reporting on the membrane environment under the conditions we propose.
**Minor comments:** - Fig 1d requires quantification We do not agree on this. This is simply to show that the labeling is dependent upon expression of the relevant ACP-IR constructs. There is no detectable labeling of the control.
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Voltage sensitivity of different PEG length of 2031-ACP probe should be added. We have added this data in figure 2 panel E.
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Fig 3a graph should show all data points, not only bar graphs. Also, the band in 3a for +CoA-PEG-NR is dimmer than other bands, is it specific to this particular gel since quantification does not show any difference?
There is no significant difference- Fig 4d, colour code is needed.
Done
- Fig 5b and Fig3d are basically the same experiments in terms of control measurement, why is the difference in 3b is 0.04 GP unit while it is 0.007 GP unit?
We explain in the MS, but have improved the title of Y-axis in Fig.5 b graph so that the difference in what is plotted is clear. - Why is inhibitor data so noisy? We should discuss.
We don’t know the exact reason why inhibitor data is noisy, but we speculate that the actin cytoskeleton and phosphoinositide-dependent signaling could affect the membrane stability, and the membrane environment would be fluctuated in the presence of latrunculin B or PI3K inhibitor.
Reviewer #2 (Significance (Required)): Overall, this is a very useful approach, and this line of research will yield very useful tools to shed light on how lipids surrounding proteins can change their function. Major advance of the paper is the new chemical biology tool. There is also biological data on how insulin can change the insulin receptor's membrane environment which is contradictory to some old literature claiming that InsR becomes more "rafty" upon insulin treatment (e.g., PMID: 11751579).
If this type of tagging proves robust and reproducible (limitations and concerns listed above and below), it could be used by other researchers to tag their protein of interest and investigate the lipid environment around those proteins.
The downside of this method is that the probe requires ACP tag, a relatively less used tag than others in biology, therefore researchers interested in using this probe should have their proteins with ACP tag. Moreover, the linker length and ACP-tag position are quite crucial parameters (and probably should be optimized for each protein). Longer PEG lengths cannot report on changes efficiently (Fig3b), while shorter lengths are prone to artefacts as they can go out of membrane (Fig1 and Fig2). This might limit its widespread use.
The reason for using the ACP tag is that neither the SNAP tap nor the HALO tag working. The tethered Nile Red preferred to bind to the tqg rather than inserting into the membrane.
**Referees cross-commenting** I agree with all comments and concerns of other reviewers. I see the usability and potential of this new technology along with its limitations as all three reviewers pointed out.
Reviewer #3 (Evidence, reproducibility and clarity (Required)): See below. No concerns on any of these issues.
Reviewer #3 (Significance (Required)): **Critique:** This MS reports a proof-of-principle for using site-directed environmentally sensitive probe technology to assess the local membrane environment of a receptor tyrosine kinase (IR) upon activation. This technology addresses a major gap in our arsenal of tools to study the mechanisms of membrane signaling as the parameters of interest are biophysical parameters rather than purely biochemical ones. How to do this with spatial and temporal resolution is a major challenge. This study builds on previous work by the Riezman group that develops an extrinsic labeling system to tether Nile Red to specific sites on the ectodomain of a signaling receptor and then probe local membrane environments as a function of receptor activity. This is a carefully done study is well-controlled, is clever in design and is well-described. Although the major issues to which such a general technology could contribute involve intracellular (and not extracellular) event, the advances described will be of general interest -- particularly that local membrane order decreases when IR becomes activated. Specific comments for the authors' consideration follow:
**Specific Comments:** (i) As a general comment, the authors are measuring extracellular plasma membrane leaflet properties that may or may not translate to what is happening in the local inner leaflet environment. A general reader may well miss the significance of this. This point needs to be more explicitly emphasized in the Discussion.
This has been discussed in the revised version.
(ii) Why not treat cells with a PLC inhibitor to block PIP2 hydrolysis and ask if that inhibits membrane disorder. It is PIP2 hydrolysis/resynthesis that regulates the actin cytoskeleton at signaling receptors and this seems an attractive candidate for study.
There is a long list of attractive post-signaling events of the insulin receptor and how this works in different cell types that could be tested. We believe that this is beyond the scope of this study and we encourage others to do this.
(iii) The data acquisition time is at least 4 min which is long enough for activated receptors to be recruited to sites of endocytosis. Can the authors exclude the possibility that what they are measuring isn't reflective of such spatial reorganization? Does a clathrin inhibitor block the observed change in local membrane order for activated IR? We determined localization to AP2 adaptor containing clathrin coated pits at the cell surface and showed that during the time-course of the experiment that there is no significant change in co-localization or evidence for endocytosis (new figure 9). Therefore, we decided not to do the clathrin inhibitor blocking experiment because we believe that it could only lead to indirect effects.
(iv) Receptor activation is accompanied by other transitions such as dimerization, etc. Can the authors exclude the possibility that what they are measuring is related to changes in depth of insertion of the NR probe into the plasma membrane outer leaflet that is a consequence of IR conformational transitions associated with activation? This is highly unlikely given the fact that fluidification of the membrane environment is found with all length linkers. Given the intervals in increases in linker length on the 2031 construct, which is the closest to the membrane, it is very difficult to conceive that any of the ones larger than 5 PEGs restrict significantly the membrane insertion of the dye. **Referees cross-commenting**
I think we have a consensus opinion
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Referee #2
Evidence, reproducibility and clarity
Summary:
In this manuscript, authors generated an ACP-attached Nile Red probe in order to specifically label Insulin receptor in the membrane. Owing to this specificity, one can measure the lipid membrane properties around a specific protein in the membrane.
Major comments:
For the conclusions in the manuscript to be convincing, in my opinion, these additional data need to be added. Some of these are new experiments, and some are detailed analysis of existing data. The new experiments are not for new line of investigation, instead it is to confirm their statements and conclusions. The major point is the reliability of spectral shift. In usual environment sensitive probes, it is certain that they are in the membrane whatever is done to the membrane. However, when the probe is attached to a protein, it is not trivial to have the same confidence that the probe is always inside the membrane, and it is in the same plane of the membrane. 1992-ACP-IR is a good example; authors state that it binds to the protein outside the membrane, but when there is cholesterol addition and -maybe more interestingly- cholesterol removal, the dye still reacts and changes its emission (even PreCT changes its emission quite a bit at the 570 nm region). This is a clear indication of a change in localization of the probe upon some changes in the membrane. This implies that observed spectral shifts may not be due to lipid packing differences, but due to localization of the probes. For this reason, it is crucial to know where any environment sensitive probe localize in the membrane with respect to membrane normal, and this knowledge is more important for this probe. Related to this, the spectral difference upon insulin treatment and activation of insulin receptor could be due to changes in probe's localization in the membrane. Especially because authors show in Fig1e, the spectra can change depending on the probe localization. Relatedly, quantum yield of NR should be significantly different when it is inside vs outside membrane. Authors should show QY for 1992-ACP-NR and 2031-ACP-NR with different PEG lengths and upon insulin treatment.
Minor comments:
- Fig 1d requires quantification
- Voltage sensitivity of different PEG length of 2031-ACP probe should be added.
- Fig 3a graph should show all data points, not only bar graphs. Also, the band in 3a for +CoA-PEG-NR is dimmer than other bands, is it specific to this particular gel since quantification does not show any difference?
- Fig 4d, colour code is needed.
- Fig 5b and Fig3d are basically the same experiments in terms of control measurement, why is the difference in 3b is 0.04 GP unit while it is 0.007 GP unit?
- Why is inhibitor data so noisy?
Significance
Overall, this is a very useful approach, and this line of research will yield very useful tools to shed light on how lipids surrounding proteins can change their function. Major advance of the paper is the new chemical biology tool. There is also biological data on how insulin can change the insulin receptor's membrane environment which is contradictory to some old literature claiming that InsR becomes more "rafty" upon insulin treatment (e.g., PMID: 11751579).
If this type of tagging proves robust and reproducible (limitations and concerns listed above and below), it could be used by other researchers to tag their protein of interest and investigate the lipid environment around those proteins.
The downside of this method is that the probe requires ACP tag, a relatively less used tag than others in biology, therefore researchers interested in using this probe should have their proteins with ACP tag. Moreover, the linker length and ACP-tag position are quite crucial parameters (and probably should be optimized for each protein). Longer PEG lengths cannot report on changes efficiently (Fig3b), while shorter lengths are prone to artefacts as they can go out of membrane (Fig1 and Fig2). This might limit its widespread use.
Referees cross-commenting
I agree with all comments and concerns of other reviewers. I see the usability and potential of this new technology along with its limitations as all three reviewers pointed out.
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jakupmichaelsen.github.io jakupmichaelsen.github.io
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Referee #3
Evidence, reproducibility and clarity
In this manuscript, the authors address the important topic of post-transcriptional gene regulation using the larval nervous system in Drosophila. They utilize a novel approach taking advantage of existing protein trap library, which permits use of the same smFISH probe to detect an array of 200 RNAs and visualize their corresponding protein expression. Furthermore, the authors developed a computational pipeline to visualize and analyze the resulting data, which should enhance the application of this method by other researchers. A major strength of the data comes from the analysis of multiple cell types in distinct compartments of the nervous system, cell types (neuron, glia, neuroblast), and subcellular domains. From the cumulative data, the authors are able to describe several interesting observations relating to cell-specific post-transcriptional regulation, regulation within a central-neuroblast lineage and glial post-transcriptional regulation, among others.
However, in spite of these strengths, there are several concerns related to the organization and interpretation of the manuscript that the authors should address in order to improve the manuscript:
General concerns:
- The approach relies on gene traps that often fail to be made homozygous, presumably due to deleterious function of the YFP insert. This is an obvious limitation of the study, which the authors address, but do so insufficiently by only analyzing a single case Dlg1. The authors should report how many of the 200 YFP-traps can produce viable homozygous animals, whether phenotypes can be observed, and any other relevant information to assess the functional properties of the tagged genes.
- The term "discordant" is used for non-congruous RNA/Protein levels in soma and distal processes, and sometimes the two are analyzed in the same figure (e.g Fig 3A). When it is stated that 98% of genes are discordant, this is an over-simplification as what the authors describe as "discordant" is expected to occur frequently in the distal process, but less often in the soma (which is what the authors find when presenting the data for individual compartments - Fig 3B-C). This is confusing because the observation means completely different things in the two compartments, though both are interesting to describe. These analyses, and their interpretation, should be kept separate.
- There is not enough emphasis placed on the cell-type specific regulation of RNAs. There are very few studies that have investigated how localization of individual RNAs changes in different cell types or regions of the nervous system, and the authors find that this is quite prevalent. Therefore, the rather superficial analysis of these data fails to take advantage of a major strength of the data. For example, for the discordant genes that differ in neuropil localization between different regions of the CNS, what types of molecules do they encode, what is their function in neurons (if known), and why might they be required locally in one region of the CNS but not the other?
- The authors conclude that mRNA and protein co-localization in glia processes shows that mRNA localization makes a major contribution of the proteome in processes. However, there is not enough evidence for such conclusion since neither translation of these mRNAs nor lack of protein trafficking from the somas was shown.
- An important caveat of this technique that should be discussed is the lack of knowledge about the translation of these mRNAs, if the mRNA that is being detected is the same as the one that is translated. While the authors emphasize the discordance between mRNA and protein localization, it is not possible to know whether these mRNAs are being translated where they are found, e.g. soma vs neuropil. Moreover, there are many examples (e.g. BDNF) where the isoform influences the subcellular localization of the mRNA. There is no way of studying the isoforms here, and we could be looking for a different mRNA isoform localized to a specific compartment compared to the protein. These points must be discussed.
Minor suggestions:
- The authors should identify GO terms to understand what types of molecules are subjected to RNA regulation. They provide a supplementary table for all genes, but it would be useful to have a chart showing the proportion of different GO terms represented in the overall gene set, genes that show cell-specific regulation, genes that show neuron vs glia specific regulation, etc.
- "However, post-transcriptional regulation can also manifest itself within a cell, so that a protein is localised to a distinct site from the mRNA that encodes it". While subcellular RNA localization may represent a regulatory layer, I do not agree that proteins that function in the cell at a different location than their translation site represents regulation per se. Many such cases exist for proteins that are trafficked!
- "The majority of individual puncta appearing in the dlg1::YFP line (51% in the brain, 64% in larval muscles". Why is the agreement between YFP and endogenous FISH so low? Do many individual RNAs fail to hybridize? This should be discussed.
- "However, one gene, indy, is highly transcribed in neuroblasts and a single ganglion mother cell before it is rapidly shut off (Figure S1A)". This figure does not exist. Where are the data?
- The authors should be consistent about calling perineurial or perineural glia (both correct) in their images and text.
- "We only observe a minority of localised axonal mRNAs that lack the protein they encode at the axon extremities, in contrast to our findings in the mushroom body, optic lobe, and ventral nerve cord neuropils" These results are not contrasted, as in all neuropils the minority of localized mRNAs are those lacking their corresponding proteins. For example, 9% in NMJ vs 7.5% in OL neuropil according to Fig. 1B. What is conflicting with the conclusion?
- "These results suggest that motor axons are more selective than the other neuronal extensions in the mRNAs that are transported over their very long distances from the soma to the neuromuscular synapse" The current literature says that the same mechanism (cis-elements) is used to transport mRNAs to subcellular compartments, which would be inconsistent with the idea of motor axons being "more selective" than other neurons for the same mRNA, but just a result of fewer mRNAs being found in motor neurons: 34.% of the mRNAs are found in motor neurons soma vs 83% in OL soma, 86.5% in VNC soma, and 70.5% in MB soma. To get to this conclusion, the authors should show that mRNAs previously found in the neuronal extensions of other neurons are not found in the axons of motor neurons but are still expressed in thesir somas. They might want to suggest different RBPs involved in the transport or discussing the very long distance they need to travel which can influence their detection in the tips. Figures
- Figure 1. Experimental approach summary
- Some colors do not show well and should be changed, e.g: grey in Fig. 1A, and Fig. 1B probe sites indicated in light blue and pink within the introns of dlg1.
- Fig. 1E': There appears to be a large discrepancy in co-detection % for CNS and muscle in the graph judging by the size of circles, yet in the text, it is stated that there is average of 51% and 64% in the two, respectively. I don't see any green circles with over 25% agreement in the graph. Are the colors correct here?
- Fig. 1D-I: It's difficult to identify where the zoomed panels come from. E has its own square (indicating zoom in E'). Please make this square dashed or a different color in E so it is clear F and G do not come from there.
- Comparing Fig. 1F vs K: Why does there appear to be so much more dlg1 mRNA in the YFP-tag condition? If this is due to selection of imaging area, please choose a more similar region to image so the RNA levels are comparable. Otherwise it indicates the YFP-tag line has more RNA expression, which is likely not the case.
- Figure 2. Analysis pipeline overview
- The lines for the first two zoomed panels are switched: The optic lobe is going to VNC and vice-versa.
- Figure 3. Overall summary of results
- Figure 3A: Soma/Neuropil/muscle should be separate or at least ordered such that they are next to each other to facilitate direct comparison of genes in the same region of the cell in neurons from different CNS areas. Why are glia not included in this summary? A third color should be used to indicate when there is neither mRNA nor protein expression.
- "Compiling all the information together shows that there are that 196/200 or 98% of the genes show discordance between RNA and protein expression" However, 5 genes shown in Fig. 3A do not show "discordance": CG9650, cup, Lasb, rg, and vsg!!
- Figure 4. Neuroblast lineage analysis
- Is clustering around the NB sufficient to determine lineage relationship? There seems to be other neurons around the NB.
- More examples should be shown for the post-transcriptional category, as it is the most interesting category, and there are many different possible outcomes. Are there cases of transcriptional control and post-transcriptional regulation? Are there cases where the youngest neurons (closer to the NB) in the progeny are expressing the protein while the oldest are not? If not, could this be an artifact from a slow translation and the protein being detected only after building up in the cell? Top1 protein (Fig. 4D) seems to be less expressed in the youngest neurons.
- "The transcription rate of these genes, as indicated by the relative intensity of smFISH nuclear transcription foci, is similar across the neuroblast lineage, however protein signal is only detectable in a minority of the progeny cells (Figure 4E)". Many nuclei lack clear large spots, but have small spots indicative of RNA; how is this interpreted? Do they lack transcription, or is this due failure of the smFISH to capture all transcription sites? Were transcripts actually counted to assess cell-specific differences? This should be possible with smFISH
- Figure 5. RNA synaptic localization
- A have global analysis comparison of all neuropil areas would be welcome in this figure.
- "Surprisingly, another 59 transcripts are present at synapses without detectable levels of protein (Figure 5E-H)" This text does not correspond to Fig 5E-H but 5I-L. Where is the text about 5E-H?
- For Fig. 5J and 5N RNA appears scattered regularly throughout the entire panel area. How sure are the authors that this is not due to poor signal/noise? For example, perhaps too much probe being used for these targets.
- Fig. 5R is not cited in the text.
- Figure 6. RNA localization in glia
- For Fig. 6B-G it is hard to tell if there is any overlap of the RNA and Glia. Maybe show multiple zoomed-in merged images and/or highlight the structures with lines that are present in all panels.
- For Fig. 6L-O: How reproducible is this small amount of RNA puncta in the NMJ glia? Is this possibly biologically important?
- Why do cartoons labelling subnuclear/perinuclear glia in Fig.6 and Fig.S6 show different localization?
- The cartoons seem to extrapolate from the data: While in Fig 6B-D, we see neither the big bright spot of transcription in the glial nucleus nor as many transcripts in the neuropil, they are both present in the cartoon. In Fig. 6E-G there is no indication of cortical glia soma nor the transcription spot only in glia nuclei.
- "To assess glial localisation for the 200 genes of interest, we used a pan-glial gal4 driving a membrane mCherry marker (repo-GAL4>UAS-mcd8-mCherry) to learn the expression pattern of all glial cells, and then classified the pattern in the YFP lines (without the marker) based on knowledge of that expression pattern. We validated this approach by combining the RFP marker" Did the authors use mCherry or RFP for these experiments? Also, the previous sentence is redundant.
- Figure 7. RNA localization at neuromuscular synapse
- RNA for these genes seems far too spread throughout the muscle to draw any conclusions
- Also with so many RNAs distributed in the muscle, specific localization of RNA molecule to the precise PSD would have no conceivable benefit
- I suggest drawing lines around the protein expression to facilitate visualization of the mRNA localization for panels B, F and J. It is especially hard to conclude anything from panels B and F.
- Light grey with white dots is hard to see in the cartoons
- Figure 8. Role of khc and activity in sgg localization
- Presumably there is a huge number of developmental problems associated with this mutant that could cause decrease in sgg localization
- If the authors include this, then they should characterize the mutant NMJs: what is the change in size, synapse number, etc..
- Is there more sgg accumulated in soma as a result of less transport? Is sgg being expressed at the same level?
- Fig. 8F-H: Why is Dlg1 accumulated in the entire axon, not just the presume synapse?
- Fig. 8J: Why is sgg signal occurring in circles disconnected from the main axon? The authors should show a different image
Significance
This is a significant and complex paper that contributes with novel tools to an important issue
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Reply to the reviewers
Manuscript number: RC-2021-01219
Corresponding author(s): Rajan, Akhila
1) General Statements [optional]
This section is optional. Insert here any general statements you wish to make about the goal of the study or about the reviews.
The goal of this study is to:
- Define how prolonged exposure to a high-sugar diet (HSD) regime alters both the lipid landscape and feeding behavior.
- Determine how changes in lipid classes within the adipose tissue regulates feeding behavior. Key findings:
In this study, by taking an unbiased systems level and genetic approach, we reveal that phospholipid status of the fat tissue controls global satiety sensing.
Impact of Key findings:
By uncovering a critical role for adipose tissue phospholipid balance as a key regulator of organismal feeding, our work raises the possibility that the rate-limiting enzymes in phospholipid synthesis, including Pect, are potential targets for therapeutic interventions for obesity and feeding disorders.
Peer review comments:
This study has immensely benefited from the thoughtful peer-review of three reviewers. As per their recommendations, we have performed a major revision by performing additional experiments (see summary table below in next section) and strived to address the major concerns raised. Based on our reading, there were two major concerns that overlapped between all three reviewers raised. They are as follows:
- Does the genetic disruption of Pect in fly fat body alter phospholipid levels? Two reviewers (#2 and #3) recommended that we perform lipidomic analyses on adult flies with adipose tissue specific knockdown of For the revised version, we have completed this lipidomic experiment, and present results as a new main Figure 6, Supplemental S7 and S9.
- Is the dampened HSD induced hunger-driven feeding (HDF) behavior because of increased baseline feeding (#1 and #3)? In addition, reviewer #1, asked us whether HSD flies experience an energy-deficit? In other words, we were asked to uncouple whether what we observed was HSD-driven allostasis or indeed, as we had interpreted, that HSD dampened hunger-driven feeding response.
Hence, they recommended that we:
- Re-analyze our hunger-driven feeding datasets and present non-normalized data (also requested by Reviewer #3) and show baseline feeding behavior on HSD. To address this, we have completed this analysis and present our results in Figure 1B-D and S1.
- Determine whether the HSD fed flies display an energy deficit on starvation. To this end, we performed an assayed starvation-induced fat mobilization on HSD, results for this are now presented on Figure 1E-G and S2. Conclusions after the revision:
First, it is important to note here that the additional experiments have not caused a significant revision of the major conclusions of the original version of our study. In fact, we hope that the revised version provides clarity and further substantiation to our original arguments.
- The lipidomics experiments on Pect fat-specific knock-down flies show that reducing Pect in fat-body causes a significant reduction in certain PE lipid species (PE 36.2 specifically- Figure 6B). This is consistent with a prior report on lipidomics of the Pect null allele by Tom Clandinin’s group (PMID: 30737130). Furthermore, we note that when Pect is knocked down in the fat body, there is a significant increase in two other classes of phospholipids LPC and LPE (Figure 6A). Together, this suggests that an imbalance in phospholipid composition in the absence of Pect activity in fat.
- The starvation-induced fat mobilization experiments show that despite being fed a prolonged HSD, adult flies sense starvation and effectively mobilize fat stores, at a level comparable to Normal food (NF) fed adult flies, suggesting that even despite HSD exposure, adult flies experience an energy deficit on starvation.
- In our non-normalized data, we find that the baseline feeding events are not significantly altered between HSD and NF-fed flies (Figure 1D). This suggests that the effects we observe are not due to an increase in the “denominator”, but a dampening of hunger-driven feeding on HSD. With regard to our original version, all three peer-reviewers found that the study was interesting, significant, important, and novel – Reviewer #1: “The work is potentially novel and interesting”; #2 : “I find the study to be potentially very important - the authors combine a longitudinal study that would be difficult in any other model with the powerful genetic tools available in the fly. The conclusions are mostly convincing”; #3: “This manuscript demonstrates how fat body Pect levels affect HSD induced changes in hunger-driven feeding response. I agree with all the reviewers points; potentially very interesting”. But had requested that we provide further substantiation and clarification.
We sincerely hope that the peer-reviewers find that our revised version with additional new experimental datasets, improved data visualization, and the presentation of non-normalized raw data points, makes this study clear, compelling, and well-substantiated.
- Point-by-point description of the revisions This section is mandatory. *Please insert a point-by-point reply describing the revisions that were already carried out and included in the transferred manuscript. *
Below we summarize in Part A, the key experiments that were performed to address the major concerns. In Part B, we provide a point-point response to each reviewer with embedded datasets.
Part a:
We performed several new experiments, including:
- To address the primary concern of Reviewer #1 regarding whether the HSD flies have a similar energy deficit to Normal food (NF) fed flies, we performed analysis of stored neutral fat Triacylglycerol (TAG) reserves and how HSD fed flies mobilized fat stores on starvation. We present these results in Figure 1E-G, S2. These results show that HSD-flies despite accumulating more TAG (S2), breakdown a similar amount of fat reserves as NF-fed flies on starvation at any time-point (Figure 1E-G). This suggests that HSD-fed flies do sense and respond to energy deficit.
- To address concerns of reviewer #2 and #3 on whether Pect genetic manipulation affects specific phospholipid classes, we performed lipidomic analyses. The table below summarizes the new 3 new figures and 4 supplemental figures (blue text are all new figure numbers and figure panels) and three new Supplementary files as per reviewer’s request.
Figure #
Main point
New datasets in revision
Companion Supplement
1
HSD alters feeding behavior, but flies still breakdown TAG on starvation.
TAG storage and breakdown over longitudinal HSD shows that HSD and NF fed flies show similar levels of TAG breakdown on starvation, despite consistently elevated TAG on HSD. This supports the idea that flies do sense starvation even on HSD, but there is a uncoupling of the feeding behavior after Day 14. Revised the data representation of Figure 1 to show non-normalized data over time. S1 and S2 companions are new in the revision. Panels 1D to 1E are new for the revision.
S1- Raw data of feeding events plotted.
S2 Elevated TAG at all time points.
2
HSD causes insulin resistance
S3A added to show that insulin transcript levels remain the same in response to reviewer #3’s concerns.
S3
3
Phospholipid concentration raw data from lipidomic on Day 7 and Day 14 HSD suggest that PC, PE levels are increased on Day 14 HSD.
Figure 3 revamped to show new data visualization and non-normalized raw data to address Reviewer #2’s major concerns. S4A and S4B added. In addition Supplementary File 1 and 2 provided with raw lipidomics data as per reviewer #2’s request.
S4.
S4A- non normalized raw data of all other lipid classes on HSD.
S4B- fatty acid species data on Day 14 added as per request of rev.#2.
4
HSD regulate Apo-I levels in the IPCs and phenocopies Pect KD.
Added Figure 4A to show that HSD phenocopies Pect-KD in terms of delivery to brain
S5 showing the validation of the Apo-I antibody.
S6 validation of Pect KD and over-expression and Pect mRNA levels dysregulation on HSD.
5
Pect RNAi is insulin resistant
N/A
N/A
6
Pect knockdown shows significant increase in LPC and LPE, and a non-significant reduction in PC, PE levels. Specifically, the PE lipid class PE36.2 is downregulated.
Fig 6, S7, S9 are completely new based on reviewer #2 and #3 requests. In addition Supplementary File 3 provided with raw lipidomics data as per reviewer #2’s request
S7, S8, S9#.
S7- new Pect KD other classes
S8- new PE classes for day 14 and Pect associated classes.
S9- Pect OE lipidomics
7
Pisd and Pect activity in adipocytes are required for hunger-driven feeding behavior in normal diets
Pisd RNAi data was moved from supplement to main figure.
N/A
Note on revised text: We have revised text not only in the results section, but also as per reviewer #2’s recommendation, we have revamped our introduction and discussion as well. Since the manuscript has been significantly revised to include a main figure 6, fully altered Figure 1 and 3, multiple new supplemental figures, the changes in text are extensive. Hence, they are unmarked in the main text. Nonetheless, we hope that the reviewers will be able to evaluate these changes, as we have provided the specific locations in text and embed key figures in the point-point response below.
__Part B: __Point-Point responses to reviewer comments.
Reviewer #1 comments in Blue, author response in black.
Reviewer #1 (Evidence, reproducibility and clarity (Required)):
In this manuscript, Kelly et al. show that the difference between the feeding behavior of fed and starved flies (hunger-driven feeding; HDF) is absent in animals fed a high-sugar diet (HSD) for two weeks or more. The disappearance of HDF with HSD coincides with changes in phospholipid profiles caused by HSD. Furthermore, RNAi-mediated downregulation of Pect in the fat body-a key enzyme in the PE biosynthesis pathway-phenocopies physiological effects of HSD. Moreover, downregulation or overexpression in the fat body abolishes or induces HDF, respectively, abolishes or induces HDF, respectively, independent of HSD treatment.
Overall, the manuscript is well-written and the phenotypes are clear. However, I have major concerns regarding the authors' interpretation of the data and their conclusion. Most importantly, while it is clear that the authors' high-sugar dietary treatment affects feeding behavior and physiology, I am not convinced that the changes can be considered "hunger-driven"-which is central to the main point of the manuscript. Therefore, it is my recommendation that the authors substantially revise the manuscript by either showing additional/re-analyzed data that rule out alternative hypotheses, or rewriting the manuscript keeping alternative interpretations in mind.
We are thankful to this reviewer for their thoughtful critique, and constructive and specific suggestions on how we can redress these concerns. We have taken on board the concerns of this reviewer regarding our interpretation of whether the changes in feeding behavior can be considered hunger-driven or not. Based on their advice, we have made significant changes by addressing: i) does HSD increased baseline feeding- we now show non-normalized raw data and data supports conclusion that baseline feeding is not higher; ii) whether HSD- fed flies can sense an energy deficit at levels similar to NF fed flies- we show that HSD flies sense energy deficit. We have provided detailed response below, and we hope the reviewer finds the additional datasets and re-analyzed data are consistent with the interpretation that prolonged HSD dampens starvation induced feeding. In addition to this key concern this reviewer has made a many other salient points that we have addressed with additional data or by clarifying the text.
Major comments: 1) The data do not sufficiently show that the long-term HSD regime disrupts "hunger-sensing." The manuscript should address alternative hypotheses by showing raw instead of normalized data, rewriting the manuscript with a new central conclusion, or running additional experiments that actually show a defect in hunger-driven response. a. The main results that the authors rely on for the argument is that the ratio of feeding events that the starved and non-starved flies eat is different between the groups fed normal or HSD. However, because the authors only show normalized data (normalized to non-starved flies; Fig. 1), it is difficult to tell whether the change is due to a chronically increased feeding in non-starved HSD flies-maybe in perpetual hunger-like allostasis-or dampened starvation response. Indeed, the data shown in Fig S1 show that flies fed HSD for as short as 5 days show more frequent feeding events compared to age-matched controls fed normal food. It is possible that because the HSD-fed flies eat more than NF-fed flies, even without being starved, the ratio of starved/non-starved feeding is lower in the HSD-fed group-due to changes in the denominator, rather than the numerator.
We have taken onboard this concern regarding presenting only normalized data, and that clouded the interpretation and left open other possibilities. In the completely revised figure 1 and S1. We now show non-normalized data, as a function of time. First we note that HSD-fed flies, do not show higher baseline feeding that NF fed flies, except on Day 10 of HSD, when there is a modest but significant elevation (Figure 1D).
Nonetheless, on Day 10 HSD, flies still display increased hunger-driven feeding HDF (Figure 1C), it is only after Day 14 HSD that HSD dampens the starvation induced feeding.
- It is also possible that the HSD-fed flies are simply not in as big an energy deficit physiologically, due to the increased fat deposits they've accumulated (as the authors show later in the manuscript). It may take longer for the fat HSD flies to reach substantial energy deficiency than the NF flies, but they still may eventually be able to appropriately respond to hunger, just like NF flies. In such case, it would be a misnomer to call this behavioral change a 'defect in hunger-driven feeding behavior.' Maybe an experiment with a dose-response curve of "hunger driven feeding response" as a function of duration of starvation would help? Prompted by this reviewers question, we asked whether HSD fed flies, that have a higher baseline neutral fat store (Triacylglycerol-TAG) level, and if HSD-fed flies can sense energy deficit. For this, we revisited the longitudinal assays for neutral fat triacylglycerol (TAG) storage that our lab had generated, along with the HSD-HDF studies. We now present this evidence as Figure 1E-1G and Figure S2. Overall, our experiments point to the idea that adult flies fed HSD, are able to sense and mobilize TAG stores effectively throughout the 28-day time point that we analysed.
First as shown in Figure S2, flies fed HSD display an increase in TAG levels. But it is to be noted that while TAG stores increase, the increase is not linear with time. This suggests that adult flies exposed to HSD store excess energy as TAG, but the increased TAG stores stay within a certain range despite the length of HSD exposure. This suggests that adult flies on HSD still display TAG homeostasis.
Next, to directly address the reviewers point about HSD fed flies not sensing an energy deficit, we subject HSD-fed flies to an overnight starvation, same regime as used in the overnight feeding experiments, and asked whether they mobilize TAG. We noted that flies exposed to HSD breakdown TAG throughout the 28-day exposure at statistically significant levels for Day 3- Day 28, except on 14 and 21 days (Figure 1F). While there is TAG mobilization on Day 14 and 21, the difference is not statistically significant. Nonetheless, we note the same levels TAG breakdown for normal lab food (NF) fed flies on Day 14 and 21 (Figure 1E). Overall, HSD fed flies sense and display energy deficit, as measured by TAG store mobilization, throughout the 28 days of HSD exposure, at levels comparable to NF-fed flies (Figure 1G).
Taken together, these results suggest that while HSD-fed flies experience an energy deficit on starvation, at levels comparable to NF-fed flies, throughout the 28-day time point assayed. But, their starvation driven feeding-response is dampened by Day 14 and by Day 28, the HSD-fed flies display more feeding events than HSD starved flies. These results are consistent with the interpretation that in HSD-fed flies the starvation-induced feeding behavior becomes desynchronized from the starvation induced TAG-mobilization, suggesting that there is an absence of hunger-driven feeding.
2) How can you be sure that lower Dilp5 immunofluorescence is indicative of increased Dilp5 secretion? Wouldn't decreased production of dilp5 also have the same results?
It has been shown previously in HSD fed larvae are hyperinsulinemic, i.e., they have 55% increase in circulating Dilp2 ( PMID: 22567167). Additionally, we have shown that ectopic activation of the insulin-producing neurons by expressing TRPA1, an ion channel that activates neurons, reduces Dilp5 accumulation without a change in Dilp5 mRNA levels (PMID: 32976758), suggesting that reduced Dilp5 accumulation, without alterations to mRNA levels is a proxy for increased secretion. Now, in response to this concern, in the revised manuscript, we have added qPCR data of Dilp2 and 5 (Figure S3A), which show no difference in expression levels after 14 days on HSD. Therefore, there is no dip in Dilp5 mRNA production. Given that Dilp2 and Dilp5 mRNA levels remain the same, but we see reduced Dilp5 accumulation, we interpret this to mean that Dilp5 secretion is increased.
- Also, the authors should state in the main text that it is Dilp5, not just any Dilp. Thanks for this suggestion and we have fixed this and referred to Dilp5 specifically throughout the text in the results section.
3) Data presentation: a. Sometimes the data are normalized to NF (Fig 4B-C), sometimes not (ex. Fig 4A, S4C). Unless there is a specific rationale for the data transformation, it would be more appropriate to show untransformed data (ex. Fig 4A, S4C), especially as the authors use two-way ANOVA to determine significance. Only showing the differences implies comparison against a hypothetical mean (i.e. μ0=0), not between two group means.
We thank the reviewers for bringing this issue to our attention. We updated all the figures to show untransformed data in the revised manuscript.
- Some figures show both individual data points and summary statistics (mean, SD, ... ex. Fig 2A)-which I believe is ideal-but some show only one or the other (ex. Fig 2B, no summary statistics; Fig. 3, no data points. The manuscript would read more convincing if data visualization is consistent across figures. We thank the reviewers for their feedback. We have made changes to all the figures in the revised manuscript to improve visual consistency.
Minor comments: 1) High sugar diet: what is the actual sugar concentration in the NF v. HSD diets? The authors write that the HSD diet contains "30% more sugar" than the NF, but providing the final sugar concentrations-sucrose or others-would be informative for other scientists studying the effect of high sugar diets.
We thank the reviewer for their suggestion and now we have updated the methods to include this sentence. “After 7 days, flies were either maintained on normal diet or moved to a high sugar diet (HSD), composed of the same composition as normal diet but with an additional 300g of sucrose per liter”.
- Additionally, the definition of HSD is inconsistent. Main text (Page 5, line 17) states that their HSD is "60% more sugar than normal media," whereas the figure legend (Fig 1) and the Methods state that the HSD contains "30% more sugar." We apologize for this egregious typo in the figure legend! We have now fixed this to say 30% HSD. Only 30% HSD was used throughout this study.
2) Starvation medium: please provide justification for why the authors used 1% sucrose/agar for starvation medium, instead of plain agar/water that most labs use. At least clarify and provide a reference for the claim that the 1% sucrose/agar "is a minimal food media to elicit a starvation response."
We are very grateful for this reviewer identifying this this methods description error and bring it to our attention. We used 0% sucrose agar for overnight starvation in this study as most labs do. The error occurred because we were using another manuscript from the lab to help draft the methods section (PMID: 29017032). In that study, where we assayed the effect of chronic starvation our lab used: “1% sucrose agar for 5 days at 25C”. However, in this current study, because we are testing acute effects of overnight starvation, we are using 0% sucrose agar.
3) Pect mRNA level is higher with HSD. This is surprising because not only, as authors mention, is increased PC32.2 with HSD suggests lower Pect activity, but also because Pect RNAi phenocopies long-term HSD in HDF behavior, lipid morphology, FOXO accumulation in fat body. The authors speculate that the data "likely shown an upregulation in an attempt to mediate the Pect dysregulation occurring at the protein level." If that were true, a western blot may be informative. Zhao and Wang (2020, PLoS Genetics) generated a Pect antibody that seems compatible with western blot applications. That being said, I don't think such data is critical for the manuscript. I mention this simply as a suggestion for the authors. a. page 8, line 22-23, did you mean to write "Given how PC32.2 is elevated after 14 days of exposure to HSD, we assumed that Pect levels would be low for flies under HSD," not "high?" Otherwise the subsequent 2 sentences don't make sense.
We agree that the most confusing aspect of the study was that Pect mRNA levels being very high on Day 14 HSD, but nonetheless the effects of Pect-KD phenocopied HSD. To resolve this, we have now performed lipidomic analyses on whole adult flies, when Pect is knocked-down (KD) by RNAi in the fat tissue. We now present a new dataset in Figure 6. Two striking changes occur. They are:
- Pect-KD shows increase in the phospholipid classes LPC and LPE (Figure 6A). In contrast, LPE is significantly downregulated on HSD Day 14 (Figure 3).
- Pect-KD shows a significant reduction in specific class of PE 36.2 (Figure 6B). Our data regarding increase in PE 36.2 agree with a previous lipidomic analyses of Pect mutant retina (PMID: 30737130). In contrast, PE 36.2 trends upwards on 14 day HSD (Figure S7C) though not significantly. On 14-day HSD consistent with extreme upregulation of Pect mRNA fed flies (Figure S6A; Pect mRNA 200-250 fold), PE trends upwards on 14-day HSD (Figure 3) and PE 36.2 trends higher (Figure S7C). We note that on the surface of it PE and LPE per se are contrasting between 14-day HSD lipidome and fat-specifc Pect-KD. But there is a significant commonality that under both states there is an imbalance of phospholipids classes PE and LPE. Hence, we propose that maintaining the compositional balance of phospholipid classes PE and LPE is critical to hunger-driven feeding and insulin sensitivity. Hence, either increase or decrease, of these key phospholipid species, may lead to abnormal hunger-driven feeding.
We agree that a western blot would be informative as well, but we were unable to obtain the reagent from Dr. Wang’s group, precluding us from performing this request. See email snapshot.
To ensure that we appropriately discuss and clarify this issue, we have now included a section in the discussion - Page 14 Lines 26-34- under the subtitle “The implications of relationship between Pect levels and HSD”. We have pasted an excerpt from that subsection below for this reviewers assessment.
“Also, we note that over-expression of Pect cDNA in the fat-body does not alter phospholipid balance (Figure S9) and indeed improves HDF on HSD (Figure 7B). While this may appear inconsistent, it is critical to note that over-expression of Pect cDNA using UAS/Gal4 only increases Pect mRNA expression by 7-fold (Figure S6A), whereas HSD causes its upregulation by 250-fold (Figure S6B). Hence, we speculate that an increased ‘basal’ level of Pect such as by that provided by a cDNA over-expression in fat, may be protective to the negative effects of HSD (Figure 7B) without affecting overall phospholipid levels (Figure S9) , but extreme upregulation Pect on HSD affects the PE and LPE balance (Figure 3).”
Reviewer #1 (Significance (Required)):
The work is potentially novel and interesting, but at this stage it's difficult to interpret what the phenotype signifies. Although the manuscript could be revised simply by modifying the text, experimentally addressing the concerns would significantly improve the work.
In sum, we hope we have addressed the key concern for Reviewer #1 as to whether the behavior we report here is indeed a dampening of starvation-induced feeding, or an effect of increase in baseline feeding. We hope that by reviewing our non-normalized data, they can appreciate that it is the former. Also, we hope that Reviewer #1 appreciates that we have strived to address the concerns by additional experiments, to clarify our findings and improve the impact of the work.
Reviewer #2 (Evidence, reproducibility and clarity (Required)):
This intriguing manuscript by Kelly and colleagues uses the fruit fly Drosophila melanogaster as a model to understand how diet-induced obesity alters the feeding response over time. In particular, the authors findings indicate that chronic exposure to a high-sugar diet significantly alters the starvation-induced feeding response. These behavioral studies are complemented by a lipidomics approach that reveals how a chronic high sugar affects many lipid species, including phospholipids. The authors then pursue mechanistic studies that indicate phospholipid metabolism within the fat body appears to remotely affect insulin secretion from the insulin producing cells. Moreover, the changes in phospholipid abundance are associated with changes in insulin-signaling, including increased insulin secretion from the IPCs and elevated levels of FOXO within the nucleus.
I find the study to be potentially very important - the authors combine a longitudinal study that would be difficult in any other model with the powerful genetic tools available in the fly. The conclusions are mostly convincing, but a few follow-up experiments are required:
We are grateful for the reviewers constructive, detail-oriented, and balanced feedback, and their recognition of the value of this study. Now, we have performed additional experiments to address the key concerns raised by all reviewers. We hope that on reading the revised version of our study, that the reviewer continues to feel positive about the message of this study and its potential impact.
- The key conclusions from the manuscript assume that manipulation of Pect expression levels alters phosphatidylethanolamine (PE) levels. However, the authors make no attempt to verify that the genetic experiments described herein actually affect PE levels. At a minimum, changes in PE levels should be verified for the Pect knockdown and overexpression lines. Similarly, there is no evidence that manipulation of either EAS or Pcyt2 induces the expected metabolic effects. I'm not asking that the longitudinal feeding experiments be repeated, simply that the authors measure the relevant lipid species, preferably with a targeted LC-MS approach.
Prompted by this reviewer, we performed targeted LC-MS on whole adult flies, on normal diet, to assess lipid levels for fat-specific Pect-KD and overexpression. We decided to focus on Pect, as its knock-down even on normal diet causes a dampened hunger-driven feeding behavior (Figure 7A) and phenocopied a 14-day HSD feeding phenotype.
We now present a new dataset in Figure 6. Two striking changes occur:
They are:
Pect-KD shows a significant reduction in specific class of PE 36.2 (Figure 6B). Our data regarding decrease in PE 36.2 agree with a previous lipidomic analyses of Pect mutant retina (PMID: 30737130). It is to be noted that though overall levels of all PE species trend downwards, like the Clandinin lab study on Pect (PMID: 30737130), we did not find a significant change in the overall PC and PE levels.
- Pect-KD shows increase in the phospholipid classes LPC and LPE (Figure 6A). In contrast, LPE is significantly downregulated on HSD Day 14 (Figure 3). On 14-day HSD consistent with extreme upregulation of Pect mRNA fed flies (Figure S6A; Pect mRNA 200-250 fold), PE trends upwards on 14-day HSD (Figure 3) and PE 36.2 trends higher (Figure S7C). We note that on the surface of it PE and LPE per se are contrasting between 14-day HSD lipidome and fat-specifc Pect-KD. But there is a significant commonality that under both states there is an imbalance of phospholipids classes PE and LPE. Hence, we propose that maintaining the compositional balance of phospholipid classes PE and LPE is critical to hunger-driven feeding and insulin sensitivity. Hence, either increase or decrease, of these key phospholipid species, may lead to abnormal hunger-driven feeding.
Finally, fat-specific Pect-OE did not cause significant changes to lipid species (Figure S9). This could either be due to the fact that in fat-specific Pect-OE flies under normal food and that we were assaying whole body lipid levels and not fat-specific lipid changes. But to counter that, even a 60% reduction in Pect mRNA levels (Figure S6A), was sufficient to produce an effect on whole body phospholipid balance (Figure 6). Hence, we speculate that by maintaining a basally higher (7-fold higher Pect mRNA level Figure S6A), might allow 14-day HSD-fed flies to buffer the negative effects of HSD and we predict that it might take longer to disrupt the phospholipid balance and HDF response.
We have now included a section in the discussion - Page 14 Lines 26-34- under the subtitle “The implications of relationship between Pect levels and HSD”. We have pasted an excerpt from that subsection below for this reviewers assessment.
“Also, we note that over-expression of Pect cDNA in the fat-body does not alter phospholipid balance (Figure S9) and indeed improves HDF on HSD (Figure 7B). While this may appear inconsistent, it is critical to note that over-expression of Pect cDNA using UAS/Gal4 only increases Pect mRNA expression by 7-fold (Figure S6A), whereas HSD causes its upregulation by 250-fold (Figure S6B). Hence, we speculate that an increased ‘basal’ level of Pect such as by that provided by a cDNA over-expression in fat, may be protective to the negative effects of HSD (Figure 7B) without affecting overall phospholipid levels (Figure S9), but extreme upregulation Pect on HSD affects the PE and LPE balance (Figure 3).”
A central hypothesis in the study is that the HSD over a period of 14 days results in insulin resistant and that these changes are leading to changes in hunger dependent feeding. I would encourage the authors to determine if Foxo mutants are resistant to these HSD-induced effects on HFD.
We thank the reviewers for this suggestion. However, given that dFOXO nuclear localization rather than expression levels regulate insulin sensitivity, we feel that disrupting dFOXO levels via mutation or knockdown will produce a plethora of indirect effects including developmental abnormalities (PMID: 24778227, PMID: 16179433, PMID: 29180716, PMID: 12893776). Our data suggest that chronic HSD treatment and Pect affect insulin sensitivity in fat tissue. However, we feel that investigating whether insulin sensitivity/FOXO signaling in fat tissue regulates feeding behavior is outside the scope of our work.
- In lines 25-30, the authors draw the conclusion that an increase in unsaturated fatty acid species is associated with the HSD and that these changes results in a more fluid lipid environment. While I agree with the model, the manuscript contains no evidence to support such a model. Either test the hypothesis or move the last line of the section to the discussion.
We thank the reviewer for this important and insightful comment. We agree that the data we presented and discussed in the original version is at the moment speculative. Addressing the hypothesis that increase in unsaturated fatty acid species result in a more fluid lipid environment will require us to build tools and expertise. Hence, this hypothesis is better suited for exploration in a future study. Given this, we have moved this out of the results section into the Discussion section titled “HSD and fat-specific PECT-KD causes changes to phospholipid profile” (See excerpt below from page 13, lines 24-35).
“In addition to changes in phospholipid classes, we found that HSD caused an increase in the concentration of PE and PC species with double bonds (Figure S4C and S4D). Double bonds create kinks in the lipid bilayer, leading to increased lipid membrane fluidity which impacts vesicle budding, endocytosis, and molecular transport14,92. Hence it is possible that a mechanism by which HSD induces changes to signaling is by altering the membrane biophysical properties, such as by increased fluidity, which would have a significant impact on numerous biological processes including synaptic firing and inter-organ vesicle transport.”
Also, as per the reviewer’s guidance, given that we are speculating here, we have also shifted this dataset from Main figure 4 to supplement S4C and S4D.
In addition, lines 25-30 state that FFAs are increased after 14 days of a HSD. Figure 3A shows the exact opposite - FFAs are significantly decreased in 14 day fed animals despite being elevated in the 7 day fed animals. This is an interesting result that warrants discussion. Moreover, I would encourage to examine the lipidomic data more carefully to ensure that the text accurately portrays the lipid profiles.
We apologize for misstating that FFAs are decreased on 14-day HSD in the lines 25-30. It was an error and we have corrected this. We agree with the reviewer that the reduction of FFA on Day 14-HSD is an intriguing and unexpected observation that needs to be emphasized and further discussed. To this end, we have added figure S4B, wherein we have provided the difference in FFA concentration (by species) after days 7 and 14.
Furthermore, we have discussed what the potential meaning of reduced FFA at Day 14 implies in page 12, lines 19-27 of the Discussion section titled “HSD and fat-specific PECT-KD causes changes to phospholipid profile”. We have stated the following-
“We speculate that this reduction in FFA maybe due to their involvement in TAG biogenesis (PMID: 13843753). We were interested to see if the decrease in FFA correlated to a particular lipid species, as PE and PC are made from DAGs with specific fatty acid chains. However, further analysis of FFAs at the species level did not reveal any distinct patterns. The majority of FFA chains decreased in HSD, including 12.0, 16.0, 16.1, 18.0, 18.1, and 18.2 (Figure S4B). This data was more suggestive of a global decrease in FFA, likely being converted to TAG and DAG, rather than a specific fatty acid chain being depleted.”
The processed lipidomics data should also be included as supplementary data table so that they can be independently analyzed by the reader.
We thank the reviewer for this suggestion. As per the reviewers request, we have included the raw data as an attachment in our supplementary material (Supplementary Files 1-3.), so that interested readers can use the datasets generated in this study for future work and further analysis.
Beyond these experimental suggestions, the manuscript needs significant editing for clarity. While I won't provide a comprehensive list, the authors need to provide accurate descriptions and annotation of genotypes (including w[1118], which is written as W1118), typos, and formatting. I've listed a few examples below:
- Page 3, Line 1 and 2: "...have been shown to impact feeding behavior and metabolism that leads to..." This is an awkward and grammatically incorrect sentence.
- Page 3, Lines 7-32 is one very large paragraph but contains concepts that should be broken down over at least three paragraphs.
- Page 3, Line 25: A description of the reaction catalyzed by Pect would be helpful for a manuscript focused on Pecte activity.
- Page 4, Line 10: "previously characterized method of eliciting diet induced feeding behavior." As stated in the text, the method is previously described yet the manuscript characterizing the method isn't cited.
- Figure legend 3 contains a random assortment of capitalized lipid species. Also, the names of lipid species are inappropriately broken into multiple names. Please use correct nomenclature throughout the manuscript.
The list above is nowhere near comprehensive. The manuscript requires significant editing.
We are grateful to the reviewer for drawing our attention to these errors. We have made significant edits to the revised manuscript to address the above-mentioned concerns, as well as made additional textual changes throughout and copyedited it. We hope that the reviewer will find the manuscript reads better and the clarity and preciseness is significantly improved.
Reviewer #2 (Significance (Required)):
I find the study to be potentially very important - the authors combine a longitudinal study that would be difficult in any other model with the powerful genetic tools available in the fly. The findings will significantly advance our understanding of how lipid metabolism links dietary nutrition with feeding behavior.
Once again, we are grateful for this reviewer’s thoughtful critique and encouraging words regarding our work and its potential impact.
Reviewer #3 (Evidence, reproducibility and clarity (Required)):
Summary: This manuscript uses Drosophila to investigate how diet-induced obesity and the changes in the lipid metabolism of the fat boy modulate hunger-driven feeding (HDF) response. The authors first demonstrate that chronic exposure (14 days) of high sugar diet (HSD) suppresses HDF response. Through lipidome analysis, the authors identify a specific class of lipids to be elevated upon chronic HSD feeding. This coincided with the changes in expression of Pect, an enzyme that regulates the biosynthesis of these lipids. Modulating the expression of Pect specifically in the fat body affected HDF response.
We thank this reviewer for their rigorous and thoughtful critique and for identifying a key issue with our original study pertaining to a gap in how Pect mRNA levels on 14-day HSD are elevated but the Pect-KD phenocopies the HDF. Now by performing whole-body adult fly lipidomic on fat-specific Pect-KD we have resolved this issue and provided clarity on role of Pect in maintaining phospholipid homeostasis and thus subsequently impacts hunger-driven feeding. We hope the reviewer finds that the revised manuscript provides further clarity to the functional link between Pect’s role in fat-body and hunger-driven feeding.
Major comments: The author claim that the HDF response in HSD is distinct between early (5d, 7d) and chronic (day 14) HSD feeding. However, the data seem to indicate that HDF response is significantly decreased at all time points in HSD. For example, at day 5 HDF response was increased only 3-fold in HSD (Figure 1C) compared to around 50-fold increase in NF (Figure 1B). The scale of the Y-axis in Figure 1B and 1C is an order of magnitude different. Including the starved data (NFstv and HSDstv) in Figure S1, normalized to NF fed group, would better visualize the overall trends. Related to this, having the source data for the actual number of feeding events would be useful (e.g., to see the baseline changes in feeding in different time points in Figure 1 and the effect of genetic manipulations in Figure 7).
As per the reviewers request, we now have modified our graphs to show source data (Figure S1) and show the raw feeding events.
Then in the non-normalized graphs we plot, over a longitudinal time course, baseline and hunger-driven feeding events (Figure 1B-D). We also show that HSD fed flies do not display increased baseline feeding (Figure 1D) suggesting that the effect we see on HDF are no clouded by increased baseline feeding.
Yes, the reviewer makes an important point that HDF response on HSD fed flies is of a lower magnitude than NF fed flies. We think that is a biologically meaningful observation, as it suggests that flies have a remarkably fine-tuned ability to coordinate food-intake with nutrient store levels.
Now we have included a paragraph in the Discussion, Page 11 Lines 23-27, that say the following to ensure the readers appreciate this salient point raised by this reviewer.
*It is to be noted that the HDF response of HSD-fed flies (Figure 1C, Days 3-10) is of lower order of magnitude than the NF-fed flies. This suggests that that in addition to sensing an energy deficit and mobilizing fat stores (Figure 1F, 1G, S1), HSD fed flies calibrate their starvation-induced feeding to compensate only for the lost amount of fat. Overall, this suggests that flies have a remarkably fine-tuned ability to coordinate food-intake with nutrient store levels. *
The association between fat body Pect level and phospholipid levels is not clear. Day 14 of HSD feeding shows high expression of Pect in the fat body and elevated levels of PC32.0 and PC32.2. The authors assume the high expression of Pect in the fat body is due to the compensatory response, but there are no data indicating downregulation of Pect levels at the earlier time points of HSD feeding. A previous study demonstrated that Pect mutant flies have lower levels of PC32.0 but higher PC32.2 (PMID: 30737130).
We agree that one puzzling aspect of the original version of this study was that Pect mRNA levels being very high on Day 14 HSD, but nonetheless the effects of Pect-KD phenocopied HSD. To resolve this, prompted by Reviewer #2 and #3 concerns, for this revised version we have now performed lipidomic analyses on whole adult flies, when Pect is knocked down (KD) by RNAi in the fat tissue. We now present a new dataset in Figure 6. Two striking changes occu. They are:
- Pect-KD shows increase in the phospholipid classes LPC and LPE (Figure 6A). In contrast, LPE is significantly downregulated on HSD Day 14 (Figure 3).
- Pect-KD shows a significant reduction in specific class of PE 36.2 (Figure 6B). Our data regarding increase in PE 36.2 agree with a previous lipidomic analyses of Pect mutant retina (PMID: 30737130). In contrast, PE 36.2 trends upwards on 14 day HSD (Figure S7C) though not significantly. On 14-day HSD consistent with extreme upregulation of Pect mRNA fed flies (Figure S6A; Pect mRNA 200-250 fold), PE trends upwards on 14-day HSD (Figure 3) and PE 36.2 trends higher (Figure S7C). We note that on the surface of it PE and LPE per se are contrasting between 14-day HSD lipidome and fat-specifc Pect-KD. But there is a significant commonality that under both states there is an imbalance of phospholipids classes PE and LPE. Hence, we propose that maintaining the compositional balance of phospholipid classes PE and LPE is critical to hunger-driven feeding and insulin sensitivity. Hence, either increase or decrease, of these key phospholipid species, may lead to abnormal hunger-driven feeding.
On day 14, HDF response was increased 70-fold in w1118 flies in NF (Figure 1B; w1118), but only 2.5-fold in lpp>LucRNAi control flies in NF (Figure 7A). This suggests that lpp-gal4 driver lines have a significant effect on HDF response. Using a different fat-body specific Gal4 line would be necessary to validate conclusions.
Regards reduced HDF magnitude, in our experience using UAS-Gal4 reduces HDF response magnitude consistently and cannot be compared to w1118 which is more robust. To account for background differences, we use Uas-Gal4 with control RNAi. It clearly shows differences in HDF response on starvation, but Pect and Pisd RNAi does not (Figure 7A). Hence, given that this experiment internally controls for any changes in HDF response for UAS-Gal4>RNAi, we conclude that HDF response in disrupted in Pect and PISD KD (Figure 7).
We only presented the Lpp-driver in our study, as this driver is the only fat-specific driver that has no leaky expression in other tissues, and is specific to fat as apolpp promoter used to generate this Gal4 line is only expressed in fat tissue (Eaton and colleagues, PMID: 22844248). Other widely used fat-specific drivers, including the pumpless-Gal4 (ppl-Gal4) driver has leaky expression in gut or other tissues (See Table 2 of this detailed study by Dr. Drummond- Barbosa https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7642949/). If the reviewer is aware of a fat-specific Gal4 line, other than Lpp-Gal4, which has a highly specific expression in the fat tissue without leaky expression in other tissues, then we are happy to take onboard the reviewer’s suggestion and try that fat-specific Gal4 that they suggest.
HSD feeding promotes Pect expression (Figure S3C) and global changes in phospholipid levels (Figure 3, 4). Therefore, shouldn't Pect overexpression (not Pect RNAi) in a normal diet mimic HSD feeding state and promote loss of HDF response? Conversely shouldn't knockdown of Pect in HSD rescue loss of HDF response?
We agree that a puzzling aspect is that Pect mRNA levels are significantly elevated in HSD Day-14, but Pect-KD showed displays the inappropriate HDF response. As we have described in our response to this reviewer on Page 19, we believe that Pect-KD and HSD disrupt PE and LPE balance overall but in different ways. Whereas Pect-OE using cDNA expression in fat body does not cause a significant change to any lipid class (Figure S9), and our results suggest that basally higher level of PECT is likely to be protective on HSD with respect to HDF(Figure 7B).
To ensure that we appropriately discuss and clarify this issue, we have now included a section in the discussion - Page 14 Lines 26-33- under the subtitle “The implications of relationship between Pect levels and HSD”. We have pasted an excerpt from that subsection below for this reviewers assessment.
“Also, we note that over-expression of Pect cDNA in the fat-body does not alter phospholipid balance (Figure S9) and indeed improves HDF on HSD (Figure 7B). While this may appear inconsistent, it is critical to note that over-expression of Pect cDNA using UAS/Gal4 only increases Pect mRNA expression by 7-fold (Figure S6A), whereas HSD causes its upregulation by 250-fold (Figure S6B). Hence, we speculate that an increased ‘basal’ level of Pect such as by that provided by a cDNA over-expression in fat, may be protective to the negative effects of HSD (Figure 7B) without affecting overall phospholipid levels (Figure S9) , but extreme upregulation Pect on HSD affects the PE and LPE balance (Figure 3).”
We would have liked to test Pect protein expression on HSD, but since we were unable to access antibodies for Pect published in a prior study (PMID: 33064773) from Dr. Wang’s lab (see Page 10-11, of response to Reviewer #1). Hence, we were unable to test how the proteins levels of Pect correlate with the 250-fold increase mRNA expression.
In conclusion, we hope the reviewer appreciates that our results regarding Pect function are consistent with the main conclusion that achieving the right phospholipid balance between PE and LPE, is critical for an organism to display an appropriate HDF response.
Minor comments: All graphs should plot individual data points and showed as box and whisker plot as much as possible.
Thanks for this suggestion, we have added individual data points to the vast majority of figures in the paper. We have made exceptions to graphs such as seen in figure 1 and FigureS4B-D where we find individual data points add an unnecessary layer of complexity. We hope these changes provide additional clarity and strength to the claims made in this manuscript.
Data for day 14 missing in Figure S4A and S4B.
We have provided Day 14 for the PC composition and PE composition, due to changes in Figures, they are now S7A and S7B.
Reviewer #3 (Significance (Required)):
The interactions between diet-induced obesity, peripheral tissue homeostasis and feeding behavior is an interesting topic that can be addressed using Drosophila. This manuscript demonstrates how fat body Pect levels affect HSD induced changes in hunger-driven feeding response. However, at this point, the functional association between fat body Pect level, global phospholipid level, and loss of hunger-driven feeding response in chronic HSD feeding is not clear.
We hope the revised data, and discussion of the paper, provides well-substantiated functional association on the importance of maintaining phospholipid balance, driven by Pect enzyme, as a critical regulator of hunger-driven feeding behavior. As stated in the revised discussion, the key take home message of our manuscript is that on prolonged HSD exposure PC, PE and LPE levels are dysregulated, the loss of phospholipid homeostasis coincided with a loss of hunger-driven feeding. Following this lead on phospholipid imbalance, we then uncovered a critical requirement for the activity of the rate-limiting PE enzyme PECT within the fat tissue in controlling hunger-driven feeding.
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Note: This preprint has been reviewed by subject experts for Review Commons. Content has not been altered except for formatting.
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Referee #1
Evidence, reproducibility and clarity
Centriole duplication is a conserved pathway that need to be tightly regulated. The key enzyme of centriole assembly is Plk4 which is recruited to the centrioles and undergoes dynamic re-localization from a ring-like pattern around a centriole to a dot-like morphology at the daughter centriole assembly site. This event is central for inducing centriole biogenesis. Plk4 then phosphorylates Ana2/STIL which allows recruitment of Sas-6 to form the cartwheel structure for centriole assembly.
In the present study, Steinacker, Wong et al. monitor how cytoplasmic concentrations of the key proteins in centriole assembly, Plk4, Asl/Cep152, Ana2/STIL, Sas-6 and Sas-4/CPAP change during the centriole assembly process in the Drosophila embryo by using fluorescence correlation spectroscopy (FCS) and Peak Counting Spectroscopy (PeCoS). They find that their concentrations remain constant with exception of Ana2/STIL of which cytoplasmic diffusion rate increased at the end of S-phase and is dependent on phosphorylation by Cdk1/CyclinB. Phosphorylated Ana2/STIL blocks centriole duplication thus preventing premature initiation of centriole duplication in mitosis.
Major comments
The manuscript is interesting and very well written. Most of the experiments are carefully performed. However, there are some important aspects for improvements that are listed below
Additional experiments:
- Figure 3: the transgenic flies that were generated here, CC and STAN, still contain wild-type Ana2. So, the authors therefore need remove or dampen their claim that the change in Ana2's cytoplasmic diffusion does not depend on its interaction with Sas-6 (page 11).
- Figure 5A: is the observed reduced recruitment of Sas-6 by Ana2(12A) due to a decrease in binding affinity? This should also be shown by analyzing protein-protein interactions between Ana2(12A) and Sas-6 biochemically.
- The authors use an Ana2(12A) mutant which comprises putative Cdk1 phosphorylation sites that have been identified in Mc Lamarrah et al. JCB 2018. However, only three of them were phosphorylated by Cdk1/cyclin B in vitro (Fig. S6). Are all these 12 putative Cdk1 phosphorylation sites important in vivo? Did the authors generate the Ana2(3A) or the S284A/T301A mutants to see whether it can rescue the ana2-/- mutant phenotype similar to the 12A mutant? These might be sufficient to observe the phenotype.
- Figure 6: is the interaction between Plk4 and Ana2(12A) impaired? Similarly, Plk4 activity and phosphorylation of Ana2(12A) by Plk4
- Figure 7: Phosphomimetics, in this case 12 amino acid changes, have the disadvantage of introducing more negative charge than the phosphorylated residue. The Ana2/(12D/E)-mNG is not efficiently recruited to centrioles. Is effect also observed for the Ana2/(3D/E) mutant?
Minor comments
Figure S1: only mNG-tagged centriolar proteins are shown. An empty mNGtag or an mNG-tagged non-centriolar protein should be shown to exclude that the tag by itself shows centriolar localization or somehow affects the localization
S4C: Sas6-mNG CPM error bars are missing for the 10min time point
S5A: What are the expression levels of the Ana2(12A) mutant? The expression levels shown in this Figure are not similar.
Significance
Centriole duplication normally begins at the G1/S phase transition. An important question in the field is how premature centriole duplication in mitosis is prevented. The authors used fluorescence correlation spectroscopy (FCS) and Peak Counting Spectroscopy (PeCoS) to study the major conserved proteins in the centriole assembly pathwayq and found that only Ana2/STIL's cytoplasmic diffusion increases at the end of S-phase. It is known from the literature that Cdk1 prevent Plk4-STIL complex assembly in centriole biogenesis by directly competing with Plk4 for the CC domain of Ana2/STIL (Zitouni et al. Curr Biol 26, 1127-1137 (2016). However, Ana2/STIL can also bind to Plk4 via its conserved C-terminal region of STIL (Ohta et al., Cell Reports 11, 2018; McLamarrah et al., J Cell Biol 2018, 217, 1217-1231). The work by Steinacker, Wong et al. suggest that at least in fly embryos, growth of the daughter centriole is regulated though phosphorylation of Ana2 by Cdk1/CyclinB rather than binding. The findings described in this manuscript are interesting for a broad range of scientists from both the centrosome and mitosis fields
Expertise of the reviewer: centriole biogenesis, structural and numerical centrosomal aberrations in disease
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hypothes.is hypothes.is
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www.devever.net www.devever.net
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The only reasonable implementation options are JavaScript and PHP.
I argue that PHP is not reasonable here. The only appropriate thing for this use case is (unminified) JS—or some other program text encoded as a document resource permitting introspection and that the user agent just happens to be able to execute/simulate.*
- Just like the advocates of "a little jQuery", author here doesn't seem to realize that the use of PHP was the first step towards what is widely acknowledged to be messed up about the "modern" Web. People can pine for the days of simple server-side rendering, but there's no use denying that today's Web is the natural result of an outgrowth that began with abuses of the fundamental mechanisms underpinning the Web—abuses that first took root with PHP.
* Refer to the fourth and sixth laws of "Sane Personal Computing, esp. re "reveals purpose"
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- Apr 2022
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github.com github.com
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www.anchormodeling.com www.anchormodeling.com
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short for peripheral data,
central to intentional software
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option for end users to reserve roles of their own
reserve roles
sounds like intent marks
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Finally, among your data, if an apperance set contains any reserved roles, then the posits containing the set are classified as peridata.
reserved roles
peridata
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Peridata between Data and Metadata
Peridata
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Tag: transitionalAll post concerning the Transitional modeling technique.
Transitional is Queen
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www.biorxiv.org www.biorxiv.org
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Author Response:
Reviewer #1 (Public Review):
The integrated stress response (ISR) controls cellular protein synthesis in response to diverse stimuli. A set of related protein kinases, with distinct regulatory domains that respond to different stress conditions, share a common kinase domain that specifically phosphorylates the translation factor eIF2 on its alpha subunit. Phosphorylation of eIF2 inhibits translation by inactivating eIF2B, the guanine nucleotide exchange factor (GEF) for eIF2. The decameric eIF2B, a dimer of heteropentamers, is the key control hub of the ISR. Previously, a small molecule inhibitor of the ISR called ISRIB was found to bind to eIF2B and was proposed to reverse the impacts of eIF2 phosphorylation by increasing stabilizing the association of eIF2B heteropentamers into the functional decameric complex. However, more recently, an alternative model ISRIB action has been proposed. eIF2B is proposed to toggle between inactivate and active states. Binding of phosphorylated eIF2 to a regulatory site is proposed to trigger the inactive state by allosterically weakening binding of eIF2 at the active site. In the new model, ISRIB has been proposed to favor the active state conformation of eIF2B and thereby overcome the effects of eIF2 phosphorylation.
In this paper, the authors further study a previously described H160D mutation in the eIF2Bbeta subunit. This mutation at one of the dimer interfaces in eIF2B was previously proposed to inhibit eIF2B by weakening dimerization. Consistent with this hypothesis, the H160D mutation impaired dimerization of eIF2B(beta, gamma, delta, epsilon) tetramers. However, in this study, the authors show that the H160D mutation does not impair dimerization when eIF2Balpha is included; thus, the mutation impairs eIF2B activity without impairing dimerization. Using biochemical assays, the authors show that the H160D mutation impairs nucleotide exchange by eIF2B decamers and weakens the binding eIF2 to eIF2B. However, the binding of phosphorylated eIF2 to eIF2B is not weakened.
Cryo-EM structural analysis of the mutant eIF2B complex reveals a partial rocking of the decameric structure that resembles the structure of the eIF2B complex when bound to its inhibitor phosphorylated eIF2. In this partially rocked structure, both the ISRIB binding site at the dimer interface and the functional eIF2alpha binding sites are widened, providing a structural solution to why the mutation weakens eIF2 binding. Interestingly, the inhibitory binding site for phosphorylated eIF2 is not affected the H160D mutation. The authors propose that the H160D mutation in eIF2Bbeta induces an allosteric conformational change that mimics the effects of phosphorylated eIF2 binding to eIF2B.
Finally, the authors generated cell lines that exclusively express the mutant eIF2Bbeta subunit. The mutation impairs total protein synthesis and cell growth rate and leads to elevated expression of the ISR marker ATF4.
This is a high-quality study, the results are convincing and the authors conclusions are supported by the data. As the ISR has been implicated in a variety of diseases, further elucidation of the mechanism of action of eIF2B and ISRIB will be critical in the development of therapeutic interventions.
A weakness of the paper (that hopefully can be easily remedied) would be to show the quality control data to verify the mutant cell lines used in Figure 6. It would be good to see that the mutant allele is present in the cells and that no WT alleles remain. In addition, examination of eIF2alpha Ser51 phosphorylation in Figure 6A would strengthen the conclusion that the eIF2Bbeta mutation is activating ATF4 expression independent of changes in eIF2 phosphorylation. Also, use of ATF4 reporters in Figure 6A, in addition to the presented Western data, would provide a nice quantitative read-out for the impact of the H160D mutation on ATF4 mRNA translation. Finally, as the biochemical and structural data indicate that the H160D mutation impairs ISRIB activity, it would be worthwhile testing whether ISRIB will rescue the slow-growth of the H160D cell lines in Figure 6D (the anticipation is that this slow-growth phenotype will not be rescued by ISRIB).
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The genotype of our cell lines at the EIF2B2 target locus was screened for by PCR + restriction enzyme digest, and later sequence verified by deep sequencing. We used the CRISPResso2 pipeline to calculate allele frequencies and HDR editing efficiencies from the sequencing data, and now also include those results in a supplementary figure (Figure 6 – supplementary figure 1).
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The levels of baseline eIF2 phosphorylation are indeed the same in WT and both H160D clones, both when assessed using a phospho-specific antibody (for eIF2alpha Ser51-P) or through band shift using phospho-retention gels (Phos-tag). We now include a new supplementary figure with this data (Figure 6 – figure supplement 3A-B).
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It is well-established in the field that ATF4 is regulated at the translational level during acute ISR activation, and indeed, reporters with the ATF4 5’ UTR have been instrumental in studying and quantifying this, allowing scientists to forego time-intensive western blots and perform high throughput analyses. Stable integration, however, can notoriously affect genomic integrity and otherwise introduce clonal variation, even when the construct is targeted to a specific locus (for example when using the FlpIn system). We have observed heterogeneity in baseline ATF4 reporter signal even when comparing polyclonal cell lines generated by lentiviral integration. As it is best practice to avoid comparing between reporter cell lines generated in different backgrounds (WT vs H160D), particularly when investigating basal conditions, we consider it more appropriate to directly measure the levels of proteins of interest by western blot, as is also commonly done in the field. By showing that ATF4 protein levels increase (Figure 6A) but its transcript levels do not (Figure 6B), while those of its target genes do (Figure 6B), we equally confirm that ATF4 is translationally upregulated in the eIF2B H160D mutant. Moreover, our Western blot conditions provide enough sensitivity to differentiate no stress (lane 1) from mild stress (lanes 5 and 9) and high stress (lanes 7 and 11). We have added notation of these specific relevant lanes to the text to make the point more accessible to the reader. We therefore consider the generation of reporter cell lines in different genetic backgrounds to be a redundant abstraction of a phenotype that we already directly show.
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Indeed, as predicted from both our in vitro and cellular work, ISRIB did not alter growth half-life of H160D cells. We included these new data in Figure 6 – supplementary figure 3C.
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www.ddbj.nig.ac.jp www.ddbj.nig.ac.jpDDBJ1
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https://github.com/lmichan/BioDBS
narid:https://www.oxfordjournals.org/nar/database/summary/1
Ya están anotadas todas las bases de datos de este hub
https://hypothes.is/search?q=tag%3ABiodatabases+https%3A%2F%2Fwww.ddbj.nig.ac.jp%2F
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- Mar 2022
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hypothes.is hypothes.is
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docs.google.com docs.google.com
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dlsoftex.com_0 : 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Author Response:
Evaluation Summary:
This work provides new insights into how surface-exposed lipoproteins of Gram-negative bacteria reach their destination in the outer membrane. Authors find that the outer membrane protein complex Slam serves as a translocon for the lipoproteins and the periplasmic chaperone Skp mediates their targeting to Slam. This work may contribute to the elucidation of host invasion mechanisms by pathogenic bacteria, in which surface lipoproteins play an important role.
Reviewer #1 (Public Review):
Previously, using rigorous genetic, bioinformatic and cell-based biochemical analyses, the same group discovered SLAM1, an outer membrane protein in Neisseria spp., which mediates the membrane translocation of surface lipoproteins (SLPs) (Hooda et al. 2016 Nature Microbiology 1, 16009). Here, authors reconstituted this system in proteoliposomes using minimal purified components including the translocon Slam1 and the client lipoprotein TbpB. Authors further coupled the system to TbpB-expressing E. coli spheroblasts and LolA, the Slam1-specific periplasmic shuttle system. Using the digestion pattern of TbpB by Proteinase K as a readout, authors confirmed that Slam1 indeed served as a translocon for SLPs. As a step forward, authors found that Skp, a periplasmic chaperone (holdase), was critical to the membrane-assembly and translocation of TbpB. Strengths: Overall, this is a solid biochemical study that demonstrates the role of Slam1 as a translocon for SLPs. The experimental design is neat and straightforward. The specific role of Skp in SLP translocation is interesting. This reconstituted system will serve as a novel platform for further elucidation of the Slam1-mediated SLP translocation mechanisms. The manuscript is overall well written. Weakness: There are several major concerns, however. 1) It is not fully convincing whether these findings are novel and significantly advance the field. Identification of minimal components in a biological process and their reconstitution are always challenging and thus, this study is an achievement. Nonetheless, I am not sure whether we have learned novel molecular insights besides the confirmation of the group's previous discovery. The specific role of Skp in translocation is interesting but not surprising, considering that periplasmic holdases are already known to be extensively involved in the biogenesis of periplasmic and outer membrane proteins.
We thank the reviewer for their time and thorough review of the manuscript. In the previous paper (Hooda et al. 2016 Nature Microbiology 1, 16009), we discovered that the outer membrane protein Slam is “important/responsible” for the surface display for SLPs (TbpB, LbpB, fHbp). In this mechanism focused manuscript, we were able to demonstrate Slam’s role as an outer membrane translocon. One of the achievements in this paper is to demonstrate that Slam as an autonomous translocon – importantly this is unlike the two-partner secretion systems, as it does not require the Bam complex for the translocation of TbpB.
2) Although authors developed nice assays (Figs. 1 and 2), it was not verified whether TbpB protected from Proteinase K digestion had "correct" conformation and membrane-topology. Authors performed a functional assay on TbpB (Fig. 5a), but this result was obtained from a cell-based assay, not from the reconstituted system.
We have performed pulldown assay for the TbpB that has been translocated into Slam-proteoliposomes using human transferrin conjugated beads to show that this TbpB protein is correctly folded and functional. Blots and explanations are attached in the revised manuscript (see new Figure 2 – figure supplement 2 and line 197-207). (As addressed in major scientific concerns point 2-i).
Although the data in Figs. 1 and 2 clearly show that the membrane association of TbpB depends on Slam1, it does not mean that the "translocation" has actually occurred in the proteoliposomes. Probably, more rigorous analysis on the Proteinase K-protected portion of TbpB (for example, mass spec) seems necessary (that is, whether the proteolytic product is expected based on the predicted topology).
The TbpB is flag-tag at its C-terminus and the protected band on our blots (detected by α-flag antibody) corresponds to the expected Mw (~75kDa) for Mcat TbpB flag tagged protein. Therefore, we believed the band at 75kDa is our full length processed TbpB. Moreover, we have confirmed that TbpB can be detected at the top of the sucrose gradient with our Slam-proteoliposomes in this assay. This would only occur if TbpB was actually translocated inside the intact liposomes, otherwise we should not see any TbpB in the top layer of the sucrose gradient (Figure 4d). Furthermore, we have performed a pulldown assay for TbpB in proteoliposomes to check for their functional binding to human transferrin beads after translocation. These results are explained in the updated new Figure 2 – figure supplement 2 and line 197-207.
3) The manuscript has a couple of missing supporting data. 3a) Lines 87-89: "From our analysis, we found that the Slam1 from Moraxella catarrhalis (or Mcat Slam1) expressed well and the purified protein was more stable than other Slam homologs." I cannot find the expression and stability data of various homologs supporting this sentence.
In general, what we meant was that we chose Mcat Slam as the target of this study because it is more stable during the purification and resulted in a higher yield of protein. We needed higher yields of Slam to be able to reconstitute the protein into the liposomes for the translocation assay. We have purification data for Mcat Slam1, Nme Slam1 and Ngo Slam2 but we think including them in the supplementary is not necessary. We have changed and rewritten this section dedicated to Mcat Slam1 purification (Figure 1 – figure supplement 1 and 2).
3b) "Lines 216-219: Furthermore, the processing of TbpB by signal peptidase II and subsequence release from the inner membrane was unaffected suggesting the defect in surface display by Skp occurs after the release of TbpB from the inner membrane (Fig. 4a)." The result supporting this sentence seems missing or this sentence points to a wrong figure.
Yes, this sentence is misleading. What we meant was that the processed TbpB (TbpB has 2 bands, unprocessed TbpB – upper band and signal peptidase processed, lipidated TbpB - lower band) is similar for all samples indicating that the knockout of Skp did not affect the expression or processing of the signal peptide of TbpB up until it is ready (processed and lipidated in the periplasm) for translocation by Slam to the surface. We have added an explanation in the figure legend of Figure 4a –line 267-269.
4) Some statistical analysis results are not clear, making some conclusions not convincing. 4a) Figure 4a top "Exposure of TbpB on the surface of K12 E. coli" Apparently, all three data points for (Delta_DegP+Slam1+TbpB) are very closely distributed. Accordingly, (WT+Slam1+TbpB) vs (Delta_DegP+Slam1+TbpB) data look significantly different (difference is ~0.2). But the two data were assigned as "Not Significant". Similarly, in the comparable in vitro data (Figure 4b), the intensity for Slam1 (WT+Proteinase K - Triton) looks larger than that for Slam1 (Delta_DegP + Proteinase K - Triton). So, the DegP contribution should not be ignored.
For figure 4a, the ONE WAY ANOVA test was performed using Prism with 4 biological replicates (we can include the analysis report in the revised submission if this is requested we have updated the figure to include data points. In general, both our in vitro liposomes translocation assay and in vivo surface exposure assay for TbpB showed that delta-DegP only slightly reduces the translocation of TbpB to the surface but could not detect statistically significant differences.
4b) Figure 5a top "Exposure of TbpB on the surface of N. meningitidis" What is the p-value for WT vs Delta_Skp data? Are the two data significantly different? The p-value range for (*) is not shown.
We have included the p-value range for (*) in the revised manuscript, figure 5a.
Reviewer #2 (Public Review):
The article addresses the function of SLAM, a protein which the authors have shown previously to be involved in the traffic of lipoproteins to the bacterial surface. The authors have performed a series of experiments to assess the impact of SLAM on the delivery into proteoliposomes of the model lipoprotein TbpB either added exogenously or presented by E coli spheroplasts. They identify a periplasmic chaperone, Skp, which enhances transport of TbpB and other lipoproteins to proteoliposomes, and show the contribution of endogenous Skp to lipoprotein transport in Neisseria meningitidis. The authors set up an in vitro translocation assays using purified components from different bacteria. This is reasonable as the assays can be challenging to establish and require proteins that can be expressed and are stable. It would be helpful however if the sources of the proteins and how they are tagged (for their detection) is clearly documented in the article and the figures. In keeping with this, the figures describing the assays could be improved (ie 1A, 2A, 3A and C). Despite this, the results presented in Fig 1 and 2 clearly demonstrate the role of SLAM as a translocase, and the authors have included appropriate controls for their assays; the translocation of a OmpA to demonstrate that the Bam complex is functional in their hands in an important control and should be included in the main figures. Experiments outlined in Figure 3 and Table 1 demonstrate the interaction specific of TbpB and another lipoprotein HpuA with Skp, a previously characterised periplasmic chaperone. This is performed by pull-downs and MS as well as immunobloting. A critical result is shown in Figure 4 in which SLAM and TbpB are introduced into E coli, and the role of endogenous Skp is assessed. Importantly, the absence of Skp reduces but does not eliminate TbpB surface expression. The authors could speculate on the nature of Skp-indendent surface expression of TbpB, as this result mirrors what they find in a meningococcal strain lacking Skp (Figure 5A). It appears that Skp might be required for the correct insertion/folding of lipoproteins given their result in Figure 5B (currently, this could be changed into 5C) which tests the binding of transferrin to the bacterial surface. Clearly this could be influenced by an effect of Skp on TbpA, which acts as a co-receptor with TbpB. In summary, the authors have used appropriate assays to reach their conclusions about the role of SLAM as a translocase and the contribution of Skp to the localisation of lipoproteins to the surface of bacteria. The findings presented are robust and shed new insights into the sorting of proteins in bacteria, an incompletely understood process which is central to microbial physiology, viurlence and vaccines.
Reviewer #3 (Public Review):
Slam was identified as an outer membrane protein involved in the translocation of certain lipoproteins to the cell surface in Neisseria meningitidis. Slam homologs were also identified in other proteobacteria. However, direct evidence that Slam is an outer membrane translocation device is still missing. In this paper, the authors set up an in vitro translocation assay to probe the role of Slam proteins in the translocation of the lipoprotein TbpB. Although they provide strong data supporting the role of Slam in lipoprotein translocation, further molecular dissection is required to unambiguously establish Slam as a lipoprotein translocator. The work is interesting and the paper clearly written. The authors also discovered a functional link between the periplasmic chaperone Skp and Slam-dependent lipoproteins, which is a novel and interesting finding.
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github-actions released this 14 Dec 2021 v0.1.6 3cdc3c3 This commit was created on GitHub.com and signed with GitHub’s verified signature. GPG key ID: 4AEE18F83AFDEB23 Learn about vigilant mode. Compare Choose a tag to compare View all tags
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blog.readwise.io blog.readwise.io
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Not only does inline tagging make it easy to add keywords and categories to your highlights, consistent use will also elevate your reading practice to the next level. Distilling a highlight down to a single keyword or forging an association between a passage and something you're working on are both forms of actively engaging with what you're reading. And actively (rather than passively) reading is essential to getting more of what you want out of books
Adding keywords isn't just to make finding things easier later on, the act of associating a highlight with a keyword or linking it to a project through a tag elevates your reading to be active rather than simply passive.
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In practice, you might not want to type out the full word .probability because typing without a keyboard can be frustrating. To help you type less, we created a shorthand feature. In the example above, you could note the passage .prob instead of .probability. The highlight would initially be tagged prob, but once you rename the shorthand a single time, Readwise will thereafter be trained to automatically convert to all .prob tags to .probability.
Readwise does tag expansion, use a shorthand tag name such as
.proband rename that in Readwise to.probabilityand from then on Readwise will expand the tag name from there. If slashes are okay in a inline tag name this would make it easy to expand.questionto.annotation/question.
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- Feb 2022
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blog.readwise.io blog.readwise.io
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Simply highlight a passage and add a note beginning with a period (.) followed by a single word or abbreviation (with no spaces).
To add a tag to an annotation simple use a
.followed by a single word to create that tag like.productivityor.InProgress.I need to find out if
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Keyword tags can help you quickly recall a passage's content, reference relevant material on a topic of interest, or identify interesting patterns in your thinking. And categorical tags can help you organize your highlights into actionable workflows for later use.
Interesting way to classify different kind of tags, keyword tags are topical while categorical tags that are associated with automated actions.
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tutorial.eyehunts.com tutorial.eyehunts.com
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HTML a name Attribute | Jump The name attribute specifies the name of an anchor tag in html. Syntax: <a name=”value”> The name attribute is used in Anchor Tag to “jump” to a specific point on a web page. It is very useful and specially used in large pages or subdivisions.
a name attribute
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Link to anchor on same page
anchor on same page
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hypothes.is hypothes.is
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A reference to the phrase "useless use of cat". See e.g. https://porkmail.org/era/unix/award.html
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hypothes.is hypothes.is
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Suppose the server were sending rel=canonical in a Link header for non-document resources (e.g. images like this one). Is the Hypothesis bookmarklet/extension thorough enough to deal with this?
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gullstothehorizon.wordpress.com gullstothehorizon.wordpress.com
- Jan 2022
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hypothes.is hypothes.is
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Name chosen as a nod to the use of Template:Should be SVG on Wikipedia
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code.flickr.net code.flickr.net
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code.flickr.net code.flickr.net
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www.biorxiv.org www.biorxiv.org
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SciScore for 10.1101/2022.01.11.475901: (What is this?)
Please note, not all rigor criteria are appropriate for all manuscripts.
Table 1: Rigor
<table><tr><td style="min-width:100px;margin-right:1em; border-right:1px solid lightgray; border-bottom:1px solid lightgray">Ethics</td><td style="min-width:100px;border-bottom:1px solid lightgray">IRB: The use of HEK293 cells in this study was approved by the University of Waterloo Research Ethics Board (ORE#42425). 2.2 Plasmids, transfections, and treatments: Plasmids expressing ORF8 protein (YP_009724396.1) tagged at the C-terminus with 3 x DYKDDDK tag (Ex-NV229-M14), ORF10 protein (YP_009725255.1) tagged at the C-terminus with 3 x hemagglutinin tag (Ex-NV231-M07), and M protein (YP_009724393.1) tagged at the C-terminus with green fluorescent protein (Ex-NV225-M03) were from GeneCopoeia (Rockland, MD, U.S.A).<br>Field Sample Permit: All work was performed in accordance with a Health Canada approved Cannabis Tracking and Licencing System Research License held by the University of Waterloo (PI: Dr. Robin Duncan).</td></tr><tr><td style="min-width:100px;margin-right:1em; border-right:1px solid lightgray; border-bottom:1px solid lightgray">Sex as a biological variable</td><td style="min-width:100px;border-bottom:1px solid lightgray">not detected.</td></tr><tr><td style="min-width:100px;margin-right:1em; border-right:1px solid lightgray; border-bottom:1px solid lightgray">Randomization</td><td style="min-width:100px;border-bottom:1px solid lightgray">not detected.</td></tr><tr><td style="min-width:100px;margin-right:1em; border-right:1px solid lightgray; border-bottom:1px solid lightgray">Blinding</td><td style="min-width:100px;border-bottom:1px solid lightgray">not detected.</td></tr><tr><td style="min-width:100px;margin-right:1em; border-right:1px solid lightgray; border-bottom:1px solid lightgray">Power Analysis</td><td style="min-width:100px;border-bottom:1px solid lightgray">not detected.</td></tr><tr><td style="min-width:100px;margin-right:1em; border-right:1px solid lightgray; border-bottom:1px solid lightgray">Cell Line Authentication</td><td style="min-width:100px;border-bottom:1px solid lightgray">not detected.</td></tr></table>Table 2: Resources
<table><tr><th style="min-width:100px;text-align:center; padding-top:4px;" colspan="2">Experimental Models: Cell Lines</th></tr><tr><td style="min-width:100px;text=align:center">Sentences</td><td style="min-width:100px;text-align:center">Resources</td></tr><tr><td style="min-width:100px;vertical-align:top;border-bottom:1px solid lightgray">Briefly, HEK293 cells were seeded (1 × 104 cells) in 96-well plates and transfected with the respective plasmids after 24 h, then treated a few hours after transfection with either CBD or vehicle for 24 h.</td><td style="min-width:100px;border-bottom:1px solid lightgray"><div style="margin-bottom:8px"><div>HEK293</div><div>suggested: None</div></div></td></tr><tr><th style="min-width:100px;text-align:center; padding-top:4px;" colspan="2">Recombinant DNA</th></tr><tr><td style="min-width:100px;text=align:center">Sentences</td><td style="min-width:100px;text-align:center">Resources</td></tr><tr><td style="min-width:100px;vertical-align:top;border-bottom:1px solid lightgray">The control plasmid was pCMV-3Tag-3A (pCMV) (Agilent Technologies, Santa Clara, CA, U.S.A.</td><td style="min-width:100px;border-bottom:1px solid lightgray"><div style="margin-bottom:8px"><div>pCMV</div><div>suggested: RRID:Addgene_16459)</div></div></td></tr><tr><td style="min-width:100px;vertical-align:top;border-bottom:1px solid lightgray">Live cells were maintained at 37° C while fluorescence was recorded at 469/525 nm for the detection of pSIVA and at 531/647 nm for the detection of PI.</td><td style="min-width:100px;border-bottom:1px solid lightgray"><div style="margin-bottom:8px"><div>pSIVA</div><div>suggested: None</div></div></td></tr><tr><td style="min-width:100px;vertical-align:top;border-bottom:1px solid lightgray">Cells were grown in 24 well plates and transfected with either pCMV-3Tag-3A, or plasmids expressing ORF8, ORF10, or M protein, and then treated with either 2 μM CBD or vehicle overnight for 14 h, so that analyses were performed prior to measures of effects on cell number and apoptosis markers.</td><td style="min-width:100px;border-bottom:1px solid lightgray"><div style="margin-bottom:8px"><div>pCMV-3Tag-3A</div><div>suggested: None</div></div></td></tr><tr><th style="min-width:100px;text-align:center; padding-top:4px;" colspan="2">Software and Algorithms</th></tr><tr><td style="min-width:100px;text=align:center">Sentences</td><td style="min-width:100px;text-align:center">Resources</td></tr><tr><td style="min-width:100px;vertical-align:top;border-bottom:1px solid lightgray">Analyses were performed using Prism GraphPad 9 software.</td><td style="min-width:100px;border-bottom:1px solid lightgray"><div style="margin-bottom:8px"><div>GraphPad</div><div>suggested: (GraphPad Prism, RRID:SCR_002798)</div></div></td></tr></table>Results from OddPub: We did not detect open data. We also did not detect open code. Researchers are encouraged to share open data when possible (see Nature blog).
Results from LimitationRecognizer: An explicit section about the limitations of the techniques employed in this study was not found. We encourage authors to address study limitations.Results from TrialIdentifier: No clinical trial numbers were referenced.
Results from Barzooka: We found bar graphs of continuous data. We recommend replacing bar graphs with more informative graphics, as many different datasets can lead to the same bar graph. The actual data may suggest different conclusions from the summary statistics. For more information, please see Weissgerber et al (2015).
Results from JetFighter: We did not find any issues relating to colormaps.
Results from rtransparent:- Thank you for including a conflict of interest statement. Authors are encouraged to include this statement when submitting to a journal.
- No funding statement was detected.
- No protocol registration statement was detected.
Results from scite Reference Check: We found no unreliable references.
<footer>About SciScore
SciScore is an automated tool that is designed to assist expert reviewers by finding and presenting formulaic information scattered throughout a paper in a standard, easy to digest format. SciScore checks for the presence and correctness of RRIDs (research resource identifiers), and for rigor criteria such as sex and investigator blinding. For details on the theoretical underpinning of rigor criteria and the tools shown here, including references cited, please follow this link.
</footer>
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- Dec 2021
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theoryofmusic.wordpress.com theoryofmusic.wordpress.com
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Beethoven’s Letters with explanatory notes by Dr. A.C. Kalischer, J.M. Dent & Sons, Ltd., London & Toronto, 1926, pp.393-394
"fuente original (secundaria)"; now, come back to esfinge
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unahistoriacuriosa.wordpress.com unahistoriacuriosa.wordpress.com
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Alejandro tenía el hábito de inclinar ligeramente la cabeza sobre el hombro derecho, de baja estatura con cutis blanco, cabello ondulado de color castaño claro y ojos heterócromos, el izquierdo marrón y el derecho gris, que no se sabe si eran de nacimiento o por un traumatismo craneal.
citation needed
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blog.readwise.io blog.readwise.io
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To use inline tagging, simply add the note .probability in addition to the highlight. When it's imported into Readwise, the passage will be tagged accordingly.
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update.lib.berkeley.edu update.lib.berkeley.eduZotero1
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Do you … ? … save random URLs in a Word or Google Doc? … save article PDFs on your desktop and as email attachments? … have a pile of article printouts sitting on your desk? … write down citations on sticky notes and post them to your monitor? … stay up late the night before a paper is due reconstructing your citations? If you answered yes to any of the above … the answer is YES, you need Zotero
zotero
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reactjsexample.com reactjsexample.com
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- Nov 2021
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compendiumofawesome.wordpress.com compendiumofawesome.wordpress.com
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Apparently, there was a poem written not too long ago by an Australian author and poet named John O’Grady[iii] entitled Tumba Bloody Rumba. I won’t include the poem here in its entirety, partly because its frequent use of the word bloody may offend some. Suffice it to say, the poem makes ample use of colourful tmesis with words such as “Tumba-bloody-rumba” and “kanga-bloody-roos.” The result, thanks in no small part to the almost hypnotic power of the word, is that tumbarumba has now become a synonym for tmesis in the English language.
tumbarumba = tmesis in Australia
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hypothes.is hypothes.is
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la omt en 1994 definió turismo como “las actividades que realizan las personas durante sus viajes y estancias en lugares distintos al de su entorno habitual, por un período de tiempo consecutivo inferior a un año con fines de ocio, por negocios y otros” (Sancho, 1998, p. 11).<
MI COMENTARIO:
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- Oct 2021
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tutorial.eyehunts.com tutorial.eyehunts.com
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HTML a tag | html anchor tag | name, link, href, target, onClick Posted April 8, 2019May 15, 2021 by Rohit
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www.biorxiv.org www.biorxiv.org
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Note: This rebuttal was posted by the corresponding author to Review Commons. Content has not been altered except for formatting.
Learn more at Review Commons
Reply to the reviewers
Note: This preprint has been reviewed by subject experts for Review Commons. Content has not been altered except for formatting.
Learn more at Review Commons
1. General Statements
We want to thank all three reviewers for their positive feedback, constructive comments, and suggestions for clarity and improvement. We are delighted to find their consensus that the manuscript represents a contribution to the field.
Accordingly, we made changes in the text (all highlighted in blue in the revised manuscript) and added a new figure as detailed in the point-by-point response.
2. Point-by-point description of the revisions
Reviewer #1 (Evidence, reproducibility and clarity (Required)):
The authors describe results of the comprehensive analysis of the prevalence and functionality of intrinsically disordered regions of the pathogen-encoded signaling receptor Tir, which serves as an illustrative example of the bacterial effector proteins secreted by Attaching and Effacing (A/E) pathogens. This is an interesting and important study that represents an impressive amount of data generated computationally and using a broad spectrum of biophysical techniques. The work serves as a model of the well-designed and perfectly conducted study, where intriguing conclusions are based on the results of the comprehensive experiments. The manuscript is well-written and concise, and I have a real pleasure reading it. The text and figures are clear and accurate.
We thank the Reviewer for these positive comments on our work.
Although, in general, prior studies are referenced appropriately, the authors should mention that the pre-formed structural elements they found in Tir are in line with the concept of "PreSMos" (pre-structured motifs) previously introduced and described in several important studies from the laboratory of Kyou-Hoon Han.
We thank the Reviewer for this suggestion. We have added a sentence to acknowledge the presence of “PreSMos” in the target-free state of Tir as putative signatures for target-binding, referring to a review article summarizing several local structural elements in unbound IDPs:
“This supports the presence of pre-structured motifs (PreSMos) as pre-existing signatures for target binding and function within target-free Tir (72)**.”
Please, note that we decided to keep this discussion to a minimum, as we cannot rule out the contribution of the induced fit model to the binding mechanism (i.e., disorder-to-order transition upon binding).
Reviewer #1 (Significance (Required)):
Solid evidence is provided that structural disorder and short linear motifs represent common features of A/E pathogen effectors. In fact, using a set of bioinformatics tools, the authors first show that although prokaryotic proteins typically contain significantly less intrinsic disorder than eukaryotic proteins, A/E pathogen effectors are as disordered as eukaryotic proteins. Using the translocated intimin receptor (Tir) as a subject of focused study, the authors then utilized a number of biophysical techniques to draw an impressive picture of disorder-based functionality. This study clearly represents a major advancement in the field of functional intrinsic disorder in general and in disorder-based functionality of proteins expressed by pathogenic bacteria. This was adds significantly to the field and will have a noticeable impact.
Again, reading this manuscript was a real joy. Finally, this work perfectly fits in the area of my expertise, since for the past 25 years or so I am working on the different aspects of intrinsically disordered proteins.
Thank you for this encouraging assessment.
**Referee Cross-commenting**
I agree with the amended recommendation of reviewer #3 to add in the manuscript EPEC O127.
According to the suggestion of Reviewer #3, we have now included EPEC O127:H6 in the manuscript.
I completely agree with comments of reviewer #2 and partially agree with reviewer #3. In my view, comparison of various strains as references for EPEC represents an interesting but independent project. It can be recommended to the authors as one of the potential future developments of their work.
Thanks for the suggestion. We are pursuing that line of research.
Reviewer #2 (Evidence, reproducibility and clarity (Required)):
The general impression is that this is an excellent study that establishes
The C-terminal intracellular region of Tir called C-Tir spanning residues 338 to 550 is largely disordered, however, observe helical structural elements involved with lipid interactions; multi-phosphorylation. The intracellular N-terminal part of Tir called N-Tir spanning residues 1 to 233 is also partially disordered but include a folded domain that is shown to assemble into a dimer
The only major concern is that no SDS-PAGE gels or size exclusion chromatograms have been included to verify purity and monodispersed of the various constructs worked on. In particular, the SAXS and CD measurement is highly sensitive to purity, and the level of degradation as IDPs are notorious for being difficult to handle in solution. it would strengthen the arguments made based that
We produced N-Tir and C-Tir as fusion proteins with a cleavable N-terminal thioredoxin tag (Trx-His6) and C-terminal Strep-tag. The latter allowed us to purify them via Strep-tag affinity chromatography as indicated by SDS-PAGE (please see Fig. S1).
We agree with the Reviewer that even small amounts of impurities (i.e., higher oligomers/degradation) can interfere with the data analysis and make interpretation of the resulting data difficult and potentially misleading. So, to avoid such problems, all samples were purified in monodispersed forms by size-exclusion chromatography (SEC) before any biophysical study.
Following the Reviewer's suggestion, we added a new supplementary figure (Fig. S5) showing the SEC-SAXS chromatogram profiles of C-Tir, N-Tir, and NS-Tir. Briefly, in the inline SEC-SAXS experiment, the sample eluates from an HPLC system directly and continuously into a BioSAXS flow cell for subsequent X-ray interrogation. Under our experimental conditions, C-Tir elutes as a single peak with Rg-values and mass compatible with a disordered monomeric protein, providing an excellent fit to the experimental SAXS curves. For N-Tir and NS-Tir, by SEC-SAXS, we separated the dimer from small amounts of high-order oligomers to yield the experimental SAXS curves of the pure dimers.
“Fig. S5. SEC-SAXS chromatograms of (A) C-Tir, (B) N-Tir, and (C) NS-Tir. Each plane shows normalized total scattering intensity I(s), over the entire s range, from each frame acquired along elution volume and respective Rg-value (black circles). The flat variation of Rg reflects a pure monodisperse sample. The column type for size exclusion chromatography and sample concentrations are on the top left of each panel. For reference, the retention volume for monomeric BSA (66.4 kDa) is displayed by red triangles.”
**Minor Comments**
Read through the manuscript to remove passages with spoken language
We thank the Reviewer for this suggestion. We went through the manuscript and improved the writing to reduce passages with spoken language.
Line 263, "To do so", should be removed
Line 290 "Our data thus" replaced with "this"
We have amended the manuscript accordingly.
Line 292 "lipid bilayers that might potentially fine-tune Tir's activity in the host cell." Weak sentence and the word fine-tune is slang. Rewrite the sentence. The interaction with lipids is fascinating!
Thanks for the suggestion. The sentence has now been changed to “**This shows that C-Tir can undergo multivalent and tunable electrostatic interaction with lipid bilayers via pre-structured elements, suggesting that membrane-protein interplay at the intracellular side might control the activity and interactions of Tir in host cells.**”
We also reinforce this fascinating message in the abstract by adding the sentence: “Membrane affinity is residue-specific and modulated by lipid composition, suggesting a previously unrecognized mechanism for interaction with the host.”
Line 192 "In figure Fig. 3A," remove the Fig
Fixed.
Line 326, "In a similar fashion," is redundant. Rewrite the sentences below.
We have modified the sentence as follows: “We evaluated whether the N-terminal cytosolic region of Tir (N-Tir; Fig S1) was also intrinsically disordered ...”
Line 342 add spaces between digit and SI unit "52kDa" there are more cases of this.
Thank you for pointing this out. This has now been corrected to 52 kDa.
Reviewer #2 (Significance (Required)):
I expect this study to have broad relevance to microbiologists working with the intimin and translocated intimin receptor, in particular the lipid interaction is likely to be followed up by the community.
We thank the reviewer for this comment. Indeed, we believe that further studies on Tir's lipid-binding ability as a novel molecular strategy in host-pathogen interactions, will potentially provide new insights on virulence, transmembrane signaling in general, and disorder-mediated functions.
**Referee Cross-commenting**
What reviewer 3 suggested in the comments sounds like added value and should be included.
I agree with reviewer 1, that the strain comparison potentially is beyond the scope presented in this manuscript.
We have now included EPEC O127:H6 in the manuscript.
Reviewer #3 (Evidence, reproducibility and clarity (Required)):
**Summary:**
This interesting manuscript look at the structure of the Nter and Cter of the effector Tir from enteropathogenic E. coli. The authors confirmed previous study highlighting the "disordered" part of the Cter. However, the extended experimental work (NMR, Small-angle X-ray scattering and CD spectroscopy) from this study also reveals the connection between different area of Tir and its implication during Tir phosphorylation and its interactions with SH2 domain.
We thank the Reviewer for this positive remark. Indeed, in our work, we highlight the structural features of the SH2-mediated interaction between Tir and host SHP-1 protein, and we also show that C-Tir is capable of lipid interaction via pre-structured motifs and that N-Tir is disordered but assembled into a dimer. Overall, we provide an updated and wide picture of Tir's intracellular side that goes beyond the scrutiny of previously described disorder features.
**Major Comments:**
The authors used E2348/69 (O127:H7) strain as a reference for EPEC. However, this strain are the least effectors of all the EPEC sequences and may over estimated the PDR in EPEC. It would be wiser to use a strain like B171 as a reference for EPEC to be able to conclude "Disordered Proteins (PDR) with long disordered regions occur in EPEC effectors similar to the human proteome". I believe that the PDR in EPEC is similar to EHEC and CR. I do not have any major concern for the rest of the work.
We thank the Reviewer for this comment. So, to clarify, we amended “EPEC” with “EPEC O127:H6” in text and figures.
We also added a paragraph at the beginning of the Discussion section to acknowledge that our prediction analysis concerns EPEC O127:H6 and two additional representative A/E bacteria strains:
“Among the enteropathogenic Escherichia coli strains EPEC O127:H6 (E2348/69) is commonly used as a prototype strain to study EPEC biology, genetics, and virulence (69). Here, we have determined the structural disorder propensity of EPEC O127:H6 sequences and two additional representatives of A/E bacteria: EHEC O157:H7 and CR ICC168.”
Finally, the Reviewer suggests to include EPEC strain B171 (serotype O111:NM) in our analysis. We agree that considering additional strains would be of value, however we believe that this is beyond the scope of this manuscript, which mainly focuses on the characterization of the structural features of the E2348/69 Tir effector. We are currently working on a broader comparative analysis among different Escherichia coli pathogenic strains, including B171, and we hope to share our findings with the community in the near future.
**Minor comments**
Statistic problem: Mann Whitney U Test (Wilcoxon Rank Sum Test) is a comparison of two independent samples with the underlying assumption is normally distributed or that the samples were sufficiently large. It is not certain that any of this assumption is correct. In addition, the effector are part of the whole proteome. Can it be then considered that both groups are independent?
We thank the Reviewer for this remark, which allows us to clarify the choice of this particular test. Indeed the Mann Whitney U-test is a non-parametric test to compare two samples with the alternative hypothesis being that one of the two samples is stochastically greater than the other. As it is a nonparametric test samples are not required to be normally distributed, as it is for the Student t-test.
Regarding the independence of the samples, when comparing the effectors collections to their corresponding proteomes, we did exclude the effectors sequences from the latter. We have clarified this point in the Supplementary Material and Methods section.
Line 120 and 442: O127 not H127
Thank you for pointing this out. It has now been corrected to O127.
Line 212: positions 409 or 405?
Yes, it should be 405. Thank you.
Reviewer #3 (Significance (Required)):
**Nature and significance:**
Tir plays a major role during EPEC infection. It is a signalling platform that has been reported to interact with multiple proteins. Whereas the extracellular part has been well characterised and crystallised, the intracellular part has been proven so far to be difficult to study. Over the last decade, no progress has been made to explain how Tir works. This manuscript provides interesting information that shade some light on how the protein could work.
**Existing literature:**
The last research manuscript trying to highlight the structural function of Tir dates from 2007 (PMC1896257). This study is far more extended and in depth than any other previous work done.
**Audience:**
the Audience may probably limited to researcher working on the field of cellular microbiology and the function associated with bacterial effector in the host. This study could be also a useful tool to identify new effectors base on their "disorder".
We thank the Reviewer for recognizing the importance of this study. We agree that our work highlights the pivotal role of disordered regions in bacterial effectors, thus enabling a better understanding of the molecular mechanisms used by pathogens to subvert the host-cell processes. We indeed believe that our work can stimulate further research on the characterization of intrinsically disordered effectors, and also beyond the cellular microbiology field, in order to gain a broader knowledge on the molecular dialogue at the host-pathogen interface, which is essential to design better therapeutic strategies.
**Expertise:**
I have been working on A/E pathogens for the last 15 years with a particular interest in Tir signalling. My domain of expertise is more in relation to cell signalling than crystallography or structural study.
**Referee Cross-commenting**
I agree with both reviewers. My comment about EPEC is more about the conclusion for some of the figures. I don't think they should conclude for the whole EPEC. The Tir variation among EHEC O157:H7 is low, but it is far more diverse for EPEC. Simply adding in the manuscript EPEC O127 should be enough.
We thank the Reviewer for this comment. As mentioned above, we now state in the manuscript, in both Results and Discussion sections, that we used E2348/69 as a representative strain for EPEC.
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- Sep 2021
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www.lewiscarroll.org www.lewiscarroll.org
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My father was talking about how Lewis Carroll’s concrete poetry was related to his experience of suffering from migraine headaches.
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hypothes.is hypothes.is
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nity-based resear
what does this mean exactly?
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docs.aws.amazon.com docs.aws.amazon.com
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With Tag Editor, you build a query to find resources in one or more AWS Regions that are available for tagging. You can choose up to 20 individual resource types, or build a query on All resource types. Your query can include resources that already have tags, or resources that have no tags.
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blog.readwise.io blog.readwise.io
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Reading at a Higher Level Not only does inline tagging make it easy to add keywords and categories to your highlights, consistent use will also elevate your reading practice to the next level. Distilling a highlight down to a single keyword or forging an association between a passage and something you're working on are both forms of actively engaging with what you're reading. And actively (rather than passively) reading is essential to getting more of what you want out of books
.tag-why .read-howto
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Keyword tags can help you quickly recall a passage's content, reference relevant material on a topic of interest, or identify interesting patterns in your thinking. And categorical tags can help you organize your highlights into actionable workflows for later use.
.c1 .tag-whyto Use both Keyword and Categorical tags.
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inline tagging — the subject of this guide — makes it even easier because adding keywords and categories in the moment is much faster than adding them after the fact.
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An inline tag is a special note taken while you read that's automatically converted into a tag in Readwise. Tagging in the moment is much faster than tagging after the fact, and once your highlights have keywords and categories, they're much easier to review and reference.
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www.biorxiv.org www.biorxiv.org
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Author response
September 9, 2021
We would like to thank ASAPbio for selecting our preprint for review! We are excited to contribute to this new process and hope others will find it as helpful as we have. The comments generated by the “crowd” were detailed and thoughtful. Below we respond to the major discussion points and if there were specific reviewer comments relevant to the discussion point, we also included that statement. We also responded to each specific comment. We would love to continue this discussion, so we invite further feedback and responses! Thanks so much for your time.
-Chelsea Kidwell, Joey Casalini, and Minna Roh-Johnson
Major Discussion Point #1:One of the most important claims is that mitochondria are the organelles responsible for the activation of the signals of cell proliferation. However, a previous report by the last author reported that macrophages transfer cytoplasm to recipient cells. It cannot be excluded that other organelles or cellular fragments are transferred as well and contribute to the observed effects (ERK activity). Perhaps a good way to solve this would be the use of macrophages that are devoid of mitochondria. At least, this aspect should be discussed in the manuscript.
🡪 We had first considered two approaches to test the requirement and sufficiency of macrophage mitochondria in cancer cell proliferation. The first was to generate rho-zero macrophages (mtDNA-deficient), as you mention in your comment, such that the macrophages did not have functional mitochondria. However, we use primary human macrophages for all of our studies, and these cells would not survive long enough to generate rho-zero cells (which requires that the cells be treated with low levels of ethidium bromide for weeks). The second is to biochemically purify mitochondria from macrophages and directly inject these mitochondrial preps into breast cancer cells. We actually did this experiment, and cancer cells injected with purified mitochondrial preps exhibited higher proliferation (by live timelapse microscopy) compared to control cells. However, we also found that the mitochondrial purifications were not clean, and contained other membranous components in the cytoplasm. We tried centrifugation-centric approaches, as well as IP-ing against a mitochondrially-localized tag, but in all cases, the mitochondrial preparations contained other cytoplasmic components. Therefore, we did not feel that this approach was an adequate way to test effects of specifically the mitochondria. We certainly wanted to discuss this aspect in the manuscript, but unfortunately, we were limited due to space. If folks have suggestions on how to best purify mitochondria, we’d love to know, so please reach out.
However, in terms of the bigger question of whether the induced proliferation in cancer cells is specifically due to ROS accumulation in transferred macrophage mitochondria, we tried to address this question with the mito-KillerRed experiments, where we generate ROS using optogenetics, and ask whether this accumulation is sufficient to induce cancer cell proliferation (which we showed it was). We also showed that this same approach could induce Erk activity, and then in separate experiments, we show that macrophage mitochondrial transfer results in accumulation of ROS and increased Erk activity. We feel that these experiments support our conclusions, however, we’d love for a way to link it all together. Unfortunately, we are not convinced that such experiments are possible at this time.
Major Discussion Point #2: Most of the positive examples of transferred mitochondria discussed appeared in a small clump. However, there also appears to be another population that was more diffuse and co-localizes with host mitochondria (e.g., Fig2B, bottom right panels). It would be helpful to show results of these sibling mitochondria for assays performed on their clumpy siblings. If they behave differently, it would be helpful to provide some explanation.
Specific Comment: Figure 2 Majority (57%) of donated mitochondria do not colocalize with LysoTracker signal (N=24 cells, 4 donors) - Here the paper implies that some transferred mitochondria do co-localize with lysoTracker signal. More importantly, they co-localize with host mitochondria. It raises the question of whether they signal through ROS and ERK like their clumpy siblings who are in the limelight of most figures.
🡪Yes, you are correct. There does appear to be a diffuse population of macrophage mitochondria. The majority of these mitochondria co-localize with lysotracker, suggesting that they are being actively degraded. We can’t say that they tend to co-localize with endogenous cancer cell mitochondria, however, it’s possible that this diffuse population is comprised of both mitochondria that are being degraded and mitochondria that are fusing with the endogenous network. We do not know if this population has a different effect on cancer cell behavior because we did not follow this population (mostly because once the mitochondria are degraded or fuse with the network, we can no longer follow those mitochondria!). However, we did follow cancer cells that contained punctate macrophage mitochondria. Often times this was the only population we could observe in the cell at that time, and this is the population in which we observe accumulated ROS.
Major Discussion Point #3:The effects that are attributed to the transferred mitochondria are highly variable (figures 1F, 3A,E) and often due to a subpopulation of samples that show a few extreme values (e.g. figures 2D, 3E, S4B, S4D). This might be expected from effects that are caused by a single mitochondria (which has a small volume) that is transferred to a complete cell. This complicates the study of the transfer process and effects and should be discussed. Also, do the authors have ideas how to improve the system, to make it more robust and easier to study the effects?
🡪The variability in the assays likely reflects the heterogeneity within the biology - Each experiment contains macrophages derived from primary monocytes that are harvested from different human blood donors! Due to the primary nature of these cells, we do expect a range of phenotypes as each donor would have a different genetic background and the monocytes were likely exposed to different environmental stimuli. In fact, even though working on this study was a giant pain due to the variability, we felt more confident about our findings because despite the heterogeneity in the system, we still observed consistent phenotypes. Below we indicate where we took a sample set and removed “outliers”, and ran the statistical tests again. The differences were still statistically significantly different, further suggesting robustness of our findings.
However, we are always on the lookout for ways to make the system easier to study. One way that we will follow up on is using M2-like macrophages since they transfer mitochondria at a higher rate than unstimulated macrophages.
Major Discussion Point #4: The authors conclude that the transfer of dysfunctional mitochondria generated a signal mediated by ROS that activates cell proliferation signals. The statement that "transferred mitochondria act as a signaling source that promotes cancer cell proliferation" is too strong. There is increased ROS production from mitochondria, yes, but an experiment in which ROS are decreased would be needed to properly sustain that conclusion. The title and abstract could be changed to better reflect the data.
Specific Comment: ‘Furthermore, treatment with an ERK inhibitor (ERKi) was sufficient to inhibit ERK activity ‘- curious as to whether antioxidant treatment would reverse any proliferative phenotypes?
🡪We wish we could quench the ROS at macrophage mitochondria. We really tried. We used a combination of ROS quenchers (NAC, mitoTempo, Tempo) and ROS readouts (mitoSOX, CellRox, DCFDA, and the 2 biosensors used in our study: Grx and Orp1), and treated cells for various amounts of time, and no matter what we tried, we could not reliably detect reduction of ROS levels in the host network or the transferred mitochondria (without killing the cells, that is). Another issue that we faced was that any pharmacological treatment would have a global effect on the mitochondrial network in the recipient cells and therefore it would not be possible to distinguish effects from global inhibition of ROS versus specifically at the site of the transferred mitochondria, and we certainly observed cell death upon treatment of ROS quenchers because of this fact. We talked to a couple of ROS experts, and they indicated that this issue is not unique to us, although we unfortunately did not have viable solutions, so if people have ideas or suggestions, please let us know!!
However, despite our failed attempts at quenching ROS, the comment that "transferred mitochondria act as a signaling source that promotes cancer cell proliferation" is too strong of a statement… well, we don’t entirely agree given that we do perform sufficiency experiments in which weinduce ROS and observe both proliferation and ERK signaling, so we do feel reasonably justified to provide the title that we did. However, we will continue to mull over this comment. Thanks for sharing your thoughts.
Major Discussion Point #5:The study may benefit from more direct evidence to support its conclusion of increased proliferation after mitochondrial transfer. While the RNA-seq, flow cytometry, counting of completion of cytokinesis and dry mass measurements provided in the present study do lend some support to the proliferation hypothesis, they all seem indirect. With the biomarkers labeling the mitochondria of donor and potential recipient cells, high content imaging and tracking of cells could be used to monitor cell division. A comparison of cell division rates of transfer-positive cells and transfer-negative cells will provide a more pertinent test of whether mitochondrial transfer promotes recipient cell proliferation.
🡪We should probably do a better job at describing the dry mass measurements (QPI, quantitative phase imaging) because we view this quantification as one of the most direct measurement to monitor cell growth/division. The approach measures the changes in dry mass as the cells prepares for cell division. So not only do we get the final readout of division (complete cytokinesis), but we also get a measure of that growth rate (the cell getting ready to divide) before cytokinesis. This is why we are so tickled to collaborate with Tom Zangle’s lab because we could finally get a direct proliferation readout in real-time. We could also use this approach to follow thousands of cells at a time, a very critical aspect since mitochondrial transfer is rare event, and therefore, we need to follow many cells to have enough statistical power to quantify the growth rates. Check out some of the Zangle lab’s other papers (PMC5866559; PMC6917840; PMC4274116), and please let us know if you disagree with us!
Major Discussion Point #6: The authors have used such a tracking-based approach on a very small scale (n=5) to measure daughter cell growth rate. However, the data do not show a statistically significant difference between the growth rates of daughters that inherited transferred mitochondria and those who did not (Fig S3). Increasing the case number via high content imaging would help obtain sufficient data points for a reliable statistical test. In addition, as suggested above, an accounting of the daughter cells' division rate for transfer positive and negative cells would provide another line of evidence to either prove or disprove the increased proliferation rate hypothesis. The same suggestion goes to the optically induced ERK activation experiments shown in Fig3F. It is also helpful to include references that studied how ERK signaling promotes proliferation and compare the evidence here with evidence or assays used in those studies as a benchmark.
Specific Comment:Figure S3 - There is no statistical test to check for ‘increase in their rate of change of dry mass over time versus sister cells that did not inherit macrophage mitochondria’. What are the colours indicative of in S3B? Can this be reported in the figure legend.
🡪You are right – the tracking-based approach on daughter cells is based on a small ‘n’. However, the tracking itself is performed on 1000s of cells. It’s just that in order to capture daughter cell data, we have to find a cancer cell with macrophage mitochondria (which is only ~1% of the population), and then follow that cell until it divides, and then follow BOTH daughter cells. So, even with the 1000s of cells that we followed, we could only capture a small number of daughter cells. The colors in S3B represent each individual triads – parent and 2 daughters. We will make this info clearer in the legend.
In terms of the optically-induced ERK activation experiments, yes, it would be great to have a higher sampling. These experiments were performed at 63x so we could reliably draw small ROIs to mimic the size of a macrophage mitochondria. While we switched to lower magnification to follow cell division, we still were limited to only a few cells for the actual photoactivation. The technical aspects of this experiment were the reason for the low sampling. Despite these limitations though, we still observed increased cell division upon mito-killerred photoactivation, which we were honestly pretty surprised (and stoked) about.
Other specific comments:
-Figure S1A - The authors could perhaps use a more aggressive gating strategy here, clipping closer to the 231 population described in Fig S1A - picking only the center of the cluster in the upper left of the RFP vs CD11b plot would likely not affect results but make them more convincing by unequivocally excluding macrophages.
-Figure 1D - Not sure about the 0.2% baseline assigned for the monoculture of cancer cells (that does not have the macrophages with the Emerald mitochondria). It is determined with cytometry - I am no expert on that topic, so maybe I missed something - but it looks weird to see some cells with transfer when there is a monoculture.
🡪Due to the variable nature of the mito-mEm signal in the recipient cancer cells (i.e. transfer of one mitochondrion vs transfer of three), we found that an overlap of 0.2% set on a fully stained monoculture control was the most accurate way to gate for the recipient cancer cells. The final gating strategies used in our study were determined by FACS-isolating populations of interest based on several different gating strategies, and directly visualizing cancer cells with macrophage mitochondria without capturing macrophages or cancer cell/macrophage fusions (which is cool, but not what we wanted). To further clarify, there is no transfer occurring in the monoculture – the overlap of mEmerald signal into the transfer gate in that control sample is likely reflective of normally occurring autofluorescence. This is a very important point, so we will make this aspect clearer in the Methods section.
-Figure S1B - Could perhaps be an interesting follow-up question for future works re: differences between cell lines and propensities to transfer mitochondria. Did the authors attempt to use other cell lines (ie, MDCK, HeLa, iPSCs, etc)?
🡪Great question and something that we have also been thinking about. To date the only recipient cells we have used are 231, MCF10A, and PDxO cells. This would be a great avenue for future studies.
-Figure S1B - Did the authors see an increase in growth rate in MCF10A line despite the lower growth rate?
🡪We have not measured the growth rate in MCF10a recipient cells but something that would be great to follow up on in future studies.
-‘physically separated from macrophages by a 0.4μM trans-well insert’ - should this read 0.4 micrometer?
🡪Yes, great catch.
-Figure S1F - The authors wrote that they used a two-way ANOVA analysis, could you report the factors used for that analysis in the Figure legend.
🡪Noted!
-Figure 1B - It is difficult to see the arrowheads in 1B, suggest moving them so they are not covering the magenta fluorescence, have them point from a different angle, and make them more brightly colored. Insets here would help the reader. A negative control image from a monoculture would also be helpful, to ensure the GFP signal is not an artifact of culture conditions.
🡪Thank you for your feedback – we will take note of this.
-Figure 1F - For graphs that do not show zero (as in 1F), the bar should be omitted. In these cases the length of the bar does not reflect the average of the data (as it does in 1D).
-Figure 3C - Please omit bar, see comment on panel 1F.
🡪 In the case of Fig 1F, we modified the y-axis to eliminate empty space. The bar is representative of mean of the data displayed in both 1D as well as 1F, but we can add a broken y-axis to help make this point.
-Figure 1 - Given that these data are fractions of a population (ie. can be described via a contingency table), isn't something like a Fisher's exact test a better measure of significance here?
🡪We think you are referring to Figure 1D? If so, we thought that we could not use Fisher’s exact test because that test assumed parametric distributions (which we do not observe). We have been working with a biostatistician for our statistics, but please do let us know if we have it wrong.
-Single cell RNA- sequencing - In the methods section the authors mention doing a differential analysis between the cells that received the mitochondria and the cells that didn’t. It might be worth introducing a figure (a heatmap or a U-MAP) relating to this analysis. Single cell sequencing would not only affirm the heterogeneity between these two populations but also help in highlighting the novel cell surface markers associated with the two populations.
🡪Yeah, good point – we can add a UMAP.
-‘mito-mEm+ mitochondria remained distinct from the recipient host mitochondrial network, with no detectable loss of the fluorescent signal for over 15 hours’- It is surprising that the transferred mitochondria do (or cannot) fuse with the host 231 mitochondria.
🡪We were also initially surprised to find that the transferred mitochondria do not fuse with the host 231 network! We think that the lack of fusion is due to the fact that the transferred mitochondria do not exhibit membrane potential (which is required for mitochondrial fusion). We also think that these results open interesting lines of questioning: Why are these depolarized mitochondria not degraded? Is this an active avoidance of the mitophagy pathway? How dynamic are these punctae? Many fun and interesting questions regarding the long-lived nature of these transferred mitochondria.
-It is unclear in these images, but the 231 mitochondria appear fragmented too. Is it possible that the mitochondrial fusion machinery (Opa1 or Mfn1/2) are inactive?
🡪231 cells are capable of fission and fusion (PMC7275541, PMC3911914, and in our own timelapse recordings), so we think that the machinery is functional. However, we don’t know whether the 231 mitochondrial machinery changes after receipt of macrophage mitochondria. Interestingly, the references above both investigate how mitochondrial dynamics promote tumor metastasis. A fascinating future direction could include an investigation to how macrophage mitochondrial transfer influences tumor cell mitochondrial dynamics.
-Figure 2B - What does the MTDR staining of the macrophage mitochondria prior to transfer look like? Important to check this to confirm that only the transferred mitochondria had lower membrane potential.
-‘significantly higher ratios of oxidized:reduced protein were associated with the transferred mitochondria versus the host network’-Here too, it would be important to check the mito-Grx1-roGFP2 readout of macrophage mitochondria prior to transfer.
🡪The way that these comments are written is as if we already know that the mitochondria are dysfunctionalbefore transfer to cancer cells. But we actually do not know if that is the case. It’s also possible that macrophage mitochondria become dysfunctional once they are in the cancer cell, which would be equally cool. So, we are actively investigating this biology.
-Figure 2A, 2BB and S1D - How were the colocalizations assessed? Was it just a visual assessment? Given the importance of these experiments for the whole story, having a quantification of the level of colocalization with each dye would be important.
🡪This is a good point and it should be straightforward to include a Pearsons coefficient for these markers.
-Figure S1D - The paper makes an argument about mitochondria transferred from Macrophages (marked green) having positive DNA stain (gray), but appearing depolarized (negative TMRM stain). The image in FigS1D is peculiar, as the majority of the 231 cells' mitochondria appear to not have any DNA stain but maintain membrane potential (positive in TMRM), while some (just above the green macrophage mitochondria) do have both DNA stain and membrane potential. The authors might want to clarify whether this is a typical scenario, and if so perhaps offer an explanation as to why the 231 mitochondria exhibit such heterogeneity.
🡪The images in S1D are of a single z-plane image therefore the DNA signal in the endogenous network is more readily visible in planes that are not shown.
-‘we confirmed that 91% of transferred mitochondria were not encapsulated by a membranous structure, thus excluding sequestration as a mechanism for explaining the lack of degradation or interaction with the endogenous mitochondrial network’ - This is based on co-staining with MemBrite 640/660, which is a dye that "covalently labels the surface of live cells", thus there is a concern as to whether this approach allows to study whether the mitochondrium is encapsulated by an endomembrane.
🡪Thank you for your feedback. We actually do think that Membrite can label endomembrane in addition to the plasma membrane. This is from the published Membrite protocol: “MemBrite™ Fix dyes are designed to be fixed shortly after staining, when they primarily localize to the plasma membrane/cell surface. Cells also can be returned to growth medium and cultured after staining, however, dye localization in live cells changes over time. Labeled membranes become internalized, so staining gradually changes from cell surface to intracellular vesicles, usually becoming mostly intracellular after about 24 hours. Internalized MemBrite™ Fix dye is usually detectable for up to 48 hours after staining, though this may vary by cell type”.
In our hands, we found that the dye started to become internalized and labeled vesicles within the cell within a few hours of staining. The images in the panels that you refer to came from time-lapse imaging experiments of between 10-15 hours, therefore the cells have internalized the MemBrite signal allowing for the visualization of internal vesicles. Also, in other studies not in the preprint, we perfused purified mitochondrial preparations onto 231 cells. The 231 cells took up the mitochondria from the environment, and all of these engulfed mitochondria were surrounded by a MemBrite positive membrane! These results further suggest that if the transferred mitochondria were encapsulated by a membrane, we would be able to visualize it.
_-‘macrophage mitochondria are depolarized but remain in the recipient cancer cell’ -_Did the authors examine the extent of cancer cell death in their co-culture system (due to the activation of apoptosis by the depolarized mitochondria)?
🡪We do not find any evidence of abnormal levels of cell death by both flow cytometry assays as well through our QPI image analysis.
-Figure 2C–D - Like in Fig 2B, in the bottom left of panel of Fig 2C there are a lot of donor mitochondria not in highly oxidized state and the growth/proliferation phenotypes apply mostly to donor mitochondria that appear 'clumpy'.
-Perhaps it is worth commenting on whether there is a link between donor mitochondrial morphology and the suspected proliferation-enhancing phenotype.
🡪The images in Fig. 2C are of the same cell – a single recipient cancer cell which is expressing the Grx biosensor. The donor mitochondria are labeled with an arrowhead, the rest of the yellow/green signal (bottom right) is from the endogenous host network and therefore we do not expect it to be in a highly oxidized state (ie. more yellow than green).
Regarding the mito morphology and proliferation – great question, and one that we are actively working on!
-‘At 24 hours, we observed a similar trend, but no statistically significant difference (Fig. S4D). These results indicate ROS accumulates at the site of transferred mitochondria in recipient cancer cells’ - if a specific sensor fails to show a significant oxidation at 24 hours compared mito-Grx1-roGFP2 which reports on mitochondrial glutathione redox state, does that mean there are ROS independent ways to oxidize Glutathione? The authors did see cell growth phenotype both in 24 and 48 hours which suggests that something is happening in 24 hours despite no significant difference in ROS H2O2 sensor.
🡪The additional biosensor that we used – mito-Orp1-roGFP2 - has been engineered to be a readout of one type of ROS – H2O2. The Grx probe is a surrogate for ROS of any type, of which there are many! To us, it is not completely unexpected that they would behave differently over time since they are readout for two separate things, and it generates an interesting possibility that different types of ROS accumulate over time. Given that the Grx probe shows an increase at 24 hours, which is when we observe the proliferation phenotype, we think we are on the right track. If you have ideas on robust ways to directly observe specific types of ROS, we would love to know!
-The differences in ratio for the two sensors used are not very convincing. In Fig 2D and Fig S4B and D the “host” and “transfer” populations are very similar. The difference seems only due to the presence of a few outliers in the “transfer” populations. More importantly, sometimes it seems that these outliers come mostly from one donor rather than being present in all 3 donors. It could be good to show histograms of the two populations for each replicate/donor and maybe redo the stats excluding these outliers.
🡪We think that the heterogeneity that is observed is due to the biology in the system – we are using primary macrophages derived from blood donors. However, for the data represented in Fig 2D, just as a test case, we took out the top four “outliers” in that data set and re-ran the Wilcoxon matched-pairs signed rank test and the p-value was 0.0010 (***), further suggesting that the ROS biosensors are revealing consistent and robust results.
-Figure S5C - it seems like the percentage of cells that divided is the same for unstimulated cells and cells with stimulated mito-KillerRed. Isn't this contrary to the expectation? The figure shows that photobleaching cytoplasm decreased % cell division, which is puzzling.
🡪The mean percent of cells that divided in unstimulated and mito bleach are very similar and was not significantly different. One point to be made that may not be well illustrated in our graphical representation is that if you look at the matched data (points connected are averaged per FOV for each condition in the same experiment) the trend shows that the mito bleach does seem to have an increase in cell division which is washed out with the average bar overlay. We should note that this experiment is very “noisy” and therefore we needed a lot of N to be able to detect significant changes. We are currently thinking about other ways to demonstrate sufficiency as it relates to cell proliferation – any experimental suggestions would be very welcome! Thanks for the feedback.
-Figure 3A - In the 'cyto' condition 6 out of 13 fields have no cells that divide. Is that expected? What is the percentage of dividing cells for cells that were not illuminated at all (a control that is lacking)? There is large variation, ranging from 0% to 22%. The evidence that illumination of KillerRed leads to increased proliferation is rather weak. Also, since Cyto and Mito are different cells, is a "paired" statistical test the right kind of test to use here?
🡪Additional data pertaining to Fig. 3A can be found in Fig. S5C, which includes the control for cells not illuminated at all. Having no cells that divide in a field of view is not surprising to us – the doubling time for these cells is ~35 hours, and we imaged for 18 hours. Also, for each field of view, our ‘n’ for each field of view was often 6-8 cells because we performed these experiments at 63X to allow for accurately drawn regions of interest for photoactivation. We also internally controlled every experiment (each experiment consisted of fields of view that had either mito activation, cyto activation, or no-activation controls, all of which were imaged overnight with multiple x/y positions). Cells that left the field of view over the 18 hours of imaging could not be quantified. It’s this sampling that caused the large variation in the graph. But again, as with many of our experiments, despite this variability, we still observe a significant difference in our experimental conditions over control cyto bleach. As for the statistical test, our understanding is that given each experiment is internally controlled, and we compare within each experiment, a paired statistical test is appropriate here. We will consult with our biostatistician to confirm, though.
-‘ROS induces several downstream signaling pathways’ - We would not expect the authors to investigate every signaling pathway, but wonder if the PI3K pathway was explored? It seems to be the other major cancer/proliferative pathway induced by ROS.
🡪Yes, this is a very good point! We actually assessed three different pathways at first – ERK, PI3K-AKT, and NLRP3/inflammasome. While analyzing these 3 pathways simultaneously, we discovered that ERK inhibitors resulted in decreased proliferation in cancer cells with macrophage mitochondria. As a result, we then focused on the ERK pathway. We still do not know if PI3K-AKT or NLRP3/inflammasome pathways play a role in this biology because we have not gone back and revisited these experiments yet, however in figure 3F, ERKi treated recipient cells exhibit a partial ‘rescue’ of baseline proliferation. This suggests that other pathways may indeed be involved and we plan to investigate this possibility.
-‘Recipient 231 cells had significantly higher cytoplasmic to nuclear (C/N) ERK-KTR ratios compared to cells that did not receive transfer’-Since two different quantification styles with opposite fraction values were used, is it possible to please specify which one was used here.
🡪Will do!
-Figure 3B - Please show the outlines of the nuclei and that of the cell.
🡪That would be helpful, wouldn’t it? Will do!
-Figure 3D - it is peculiar that ERK-KTR in Fig 3D is so strongly cytosolic while in Fig 3B it is almost exclusively nuclear. If this sensor behaves differently in different situations, the authors may want to comment on how that would affect their conclusions.
🡪The panels in Fig. 3B were taken with the ImageStream flow cytometer which takes a lower resolution image of a single plane of a cell in suspension in the flow stream. In Fig. 3D, those images are from confocal spinning disk microscopy which allows for higher resolution, z-stack images of adherent cells on glass. Therefore, we think the differences that you point out are likely due to the fact that the two images come from very different imaging systems.
-Figure 3E - The effect of 'opto-induced' ERK activity is weak. The initial ERK-KTR is 1 at time point zero (as the data is normalized to this timepoint) and around 1 for both the cyto and mito condition. A statistical difference is observed, but the effect is minor and it is unclear whether it is biologically meaningful. The 'cyto' condition shows an average below 1 and the mito condition remains 1, suggesting that ERK activity remains constant when ROS are produced in the mitochondria.
-Also from S8C and 3E it appears cyto actually shows a decrease rather than mito showing an increase, could the authors comment on this?
🡪We have a few thoughts on this. The first is that we don’t expect a dramatic change in ERK signaling because the ROS accumulation is localized to a small region in the recipient cell. This is not a situation where we would expect a large-scale change because we are adding a growth factor. We can understand that the change in ERK activity may appear to be minor, but our data suggest that these subtle changes in kinase signaling translate into significant changes in downstream behavior – proliferation. The way that we interpret differences as “biological meaningful” is whether they exhibit a functional response, and in our study, we show that inhibiting the induction of ERK activity in cancer cells with macrophage mitos inhibits proliferation. What is most interesting to us is that cancer cells that do not have macrophage mitochondria have an unchanged fraction of cells in G2/M phase of the cell cycle in response to the concentration of ERK inhibitor we used, suggesting that the ERK inhibition specifically blocks macrophage mitochondria-induced proliferation.
In Fig. S8C, bleaching a region of cytoplasm does seem to cause a decrease in ERK activity over time. We really can’t explain this result. However, we do think that ERK activity is higher in mito-bleached cells because mt-ROS is generating an increase in ERK activity which compensates for the decrease in activity that occurs when the cytoplasmic region of interest is photobleached. It’s still a head scratcher, though, but we did perform internal controls for every experiment (as we describe above), and the mito-bleach, cyto-bleach, and no-bleach conditions were run side-by-side such that we can make apples-to-apples comparisons.
-‘patient-derived xenografts (PDxOs)’ - As a control it would be relevant to include a normal mammary organoid model perhaps from the same patient to demonstrate that the transfer of mitochondria specifically to the cancer cells is more beneficial.
🡪Using a normal mammary organoid cells as a control to compare efficiency of transfer and downstream phenotypes would be very interesting. Due to the fact that these are patient-derived organoids, we are unable to acquire non-malignant cells from the same patient. Expanding our studies in the MCF10A cell line that we utilized in this paper would be an alternative to what you propose and would also expand our understanding of general biology underlying mitochondrial transfer.
-‘macrophages to both HCI-037 and HCI-038 PDxO cells (Fig. 4G)’ - Why is M0 able to transfer efficiently to HCL-037 tumour when its mitochondrial network is less fragmented as M2?
🡪These results really stood out to us. It was quite surprising that in HCI-037, both M0 and M2 macrophages were able to transfer their mitochondria at similar efficiencies, but in HCI-038, M2 macrophages were more efficient at transfer. HCI-037 is a primary tumor, and HCI-038 is a metastases from the same patient, so there are some exciting avenues of study to examine how macrophage mitochondria transfer differs at the primary versus metastatic site. There is still very little known about how donor cell dynamics influence mitochondrial transfer!
-Are mito transfer from M0 depolarised and accumulate ROS or show increased ERK activity or increased cell proliferation?
🡪Yes – all studies, except studies pertinent to fig 4 (where we assessed macrophage differentiation states), were done with M0 macrophages.
-‘M2-like macrophages preferentially transferred mitochondria to the bone metastasis PDxO cells (HCI-038) when compared to primary breast tumor PDxO cells (HCI-037)’ -The authors may want to check this statement here as it is in consistent with their data plot. In Fig. 4G, M2/PDxO transfer percentages for HCI-037 and HCI-038 are about the same, unless the authors provide statistical tests to prove otherwise. Instead, M0 appears to transfer mitochondria to HCI-037 much more efficiently than it does HCI-038.
🡪Upon re-reading our sentence again, we now realize that it’s actually quite poorly written, so we can understand the confusion! What we meant to articulate is that M2-like macrophages are better at transferring mitochondria to HCI-038 than M0 macrophages. Whereas in HCI-037, we do not observe the same preferential transfer (ie. M0 and M2 can transfer at the same efficiency). We will certainly clarify this language in the manuscript.
-‘M2-like macrophages exhibit mitochondrial fragmentation’ - Is there a correlation between the status of the mitochondrial network in the donor and the % of transfer to the recipient? If so, this would be a correlation that would support the conclusions.
🡪Yes, please see Fig. 4C for transfer rates with different donor subtypes and Fig. 4H for a general working model on how we think these data fit into the larger picture.
-‘accumulate ROS, leading to increased ERK activity’ - Did the authors obtain similar results with the PDXOs? It would be an interesting observation if the primary samples also exhibit a mechanism similar to established cell lines wherein there are more accumulated genetic changes.
🡪Our main limitation with PDxOs is overcoming the technical hurdles related to our downstream assays. These include introducing relevant reporters and generating stable lines in the PDxOs, and imaging at high-resolution when the PDxOs are cultured in 3D. However, we are very interested in this question as well, and are actively thinking about ways to overcome these hurdles.
-It would also be interesting to examine whether there is any difference in the ROS-ERK mechanism for primary and metastatic tumour.
🡪We agree and this is an active avenue of investigation for us. We agree and are currently pursing models to understand how our findings fit into the larger picture of tumorigenesis and metastatic potential. We had spent months pursuing anin vivo approach using a murine Cre/LoxP system to genetically label mouse macrophage mitochondria with GFP. We crossed mice which express Cre under a monocyte-specific promoter (Jax, SN: 004781) and mice with germline expression of Lox-Stop-Lox-3xHA-EGFP-OMP25 (Jax, SN: 032290) with the expectation of seeing Cre-based excision of the stop cassette – thus resulting in offspring with macrophages expressing mitochondrial-localized GFP. However, the macrophages of the resulting offspring do not express GFP (by flow cytometry, imaging, and western blot analysis), despite the PCR-verified presence of both transgenes and the excision of the stop cassette. Needless to say, this was quite frustrating! We are currently in the process of developing a newly available MitoTag model which has been optimized for visualization purposes (Jax, SN: 032675). If you have any suggestions or advice on this matter we would much appreciate your thoughts!
-‘in cancer cells that receive exogenous mitochondria’ - Since these macrophages also transfer mitochondria to non-malignant cells, such as MCF10A cells shown in Fig S1B, perhaps the authors could comment on whether this is part of a physiological process that would also promote normal cell growth?
🡪 There are so many questions regarding when and why macrophages might transfer mitochondria. In general, mitochondrial transfer is observed in stressed cells. Our data suggest that transfer happens to MCF10A cells although at a much lower rate than their malignant counterparts, 231 cells, but we do not know whether similar downstream mechanisms and phenotypes are also occurring in the non-malignant cells. Thanks for your feedback – more to come here!
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stackoverflow.com stackoverflow.com
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target="_blank" which opens the anchor in a new window(which has been redirected to tabs by browser settings usually)
new window => new tab
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Instead if this anchor was nested in frames it would open in a sandbox mode of sorts, meaning only in that frame.
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- Aug 2021
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www.makeuseof.com www.makeuseof.com
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5. Foreground and Background
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4. Leading Lines
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3. The Principles of Gestalt
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2. The Golden Ratio
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1. The Rule of Thirds
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www.makeuseof.com www.makeuseof.com
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4. With One Lens, Shoot 1,000 Photos
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2. With One Subject, Shoot 10 Photos
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1. Crop Someone Else's Photos
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jessitron.com jessitron.com
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symmathesy
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www.makeuseof.com www.makeuseof.com
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Check that not in cloud 1st. Can't I just delete from cloud as well?
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www.bz-berlin.de www.bz-berlin.de
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Bereits im März war das Besuchsrecht in Krankenhäusern und Pflegeheimen der Hauptstadt stark eingeschränkt worden.
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wiki.c2.com wiki.c2.com
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The resilience of any such ecosystem is equal to it's diversity + interconnectedness.
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instructionalalchemy.com instructionalalchemy.com
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more
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Transprovenance
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- Jul 2021
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Task related plugin for Obsidian.
<small><cite class='h-cite via'>ᔥ <span class='p-author h-card'>Eleanor Konik</span> in 2021-07-17: Obsidian Mobile, Community Events & Graph Tips (<time class='dt-published'>07/29/2021 11:06:38</time>)</cite></small>
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www.biorxiv.org www.biorxiv.org
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Note: This rebuttal was posted by the corresponding author to Review Commons. Content has not been altered except for formatting.
Learn more at Review Commons
Reply to the reviewers
Dear reviewers,
We thank all reviewers for and their appreciation of our work and even more so for their constructive comments and suggestions, which will significantly improve the quality of the manuscript. We were able to complete the revision and address all reviewer comments. Aside a more stringent discussion of the literature, and rewording of certain paragraphs for clarity, we also generated additional experimental data.
More importantly, to address the concern that we did not provide a positive marker for the intranuclear compartment, we present new images. We attempted to label gamma-Tubulin by generating new antibodies, GFP-tagged strains, and trying multiple commercial antibodies since the beginning of the project. Only recently we found an antibody providing a more specific signal at the expected location, although with some likely cross-reactivity with alpha- and beta-tubulin, and now show these data in the supplements. Additionally, we generated expansion microscopy samples stained with a fluorophore-coupled NHS-Ester, a bulk protein label. These data show that the centrosome contains an exceptionally protein dense hourglass-shaped region, which spans from the extranuclear to the intranuclear compartment, as revealed by centrin and tubulin co-staining. This fortifies our claims about the distinct nature of the intranuclear centrosome compartment containing the microtubule nucleation sites.
Further, we add images of 5-SiR-Hoechst, SPY555-Tubulin, Centrin1-GFP triple labelling live cells to demonstrate the specificity of the microtubule dye and to underline that we are indeed acquiring the dynamics from the first nuclear division on.
In terms of formatting we added line numbers and uploaded high quality figures separately. Due to the added data and panels we needed to split Fig. 1 into two separate figures, rewrote the figure legends and moved them to the end of the document.
Please find below a point-by-point response to the comments.
Best regards,
Julien Guizetti
Reviewer #1 (Evidence, reproducibility and clarity (Required)):
The manuscript by Simon and collaborators addresses the dynamic changes of spindle and hemi-spindle microtubules occurring along schizogony in Plasmodium falciparum. The work explores the temporal correlation of the changes observed in intranuclear spindles with changes at the level of the centriolar plaque; the nuclear microtubule organizing center of these parasites, using centrin as a bona fide marker of the structure. The study shows that spindle microtubules organize from an intranuclear region, devoid of chromatin, distinct from the centrin region which had not been observed or described before. It further shows that centrin does not localize at the nuclear envelope, but it is actually extranuclear.
This work significantly expands on previous knowledge regarding the functional and spatial organization of the nucleus in P. falciparum, and the structure once defined as "an electron dense mass on the nuclear envelope." It uses state of the art microscopy approaches such as STED, UExM and CLEM, in combination with immunolabeling, dyes and parasites over expressing fluorescent protein fusions, to address these questions.
**Major comments:**
- Are the key conclusions convincing?
I find the manuscript successfully addresses the posed questions. The data presented supports the conclusions.
Should the authors qualify some of their claims as preliminary or speculative, or remove them altogether?
Would additional experiments be essential to support the claims of the paper? Request additional experiments only where necessary for the paper as it is, and do not ask authors to open new lines of experimentation.
No
- Are the suggested experiments realistic in terms of time and resources? It would help if you could add an estimated cost and time investment for substantial experiments.
N/A
- Are the data and the methods presented in such a way that they can be reproduced?
Yes
- Are the experiments adequately replicated and statistical analysis adequate?
Yes
**Minor comments:**
- Specific experimental issues that are easily addressable.
On the data shown in Figure 1, it is unclear to me what elements are taken into account to define "anaphase." Anaphase could be defined by using chromatin markers - such as CenH3- which have been identified in Plasmodium and the authors make use of in Figure 1F.
We acknowledge that the term anaphase is ill-defined here. Further it suggests a mitotic morphology analogous to the one observed in “classical” models (prophase, metaphase, anaphase,…), which is not fully appropriate. In line with the comments by Reviewer 3 we, therefore, decided to use the term “extended spindle” instead (Fig. 1 & 2). This better reflects the morphological criterion on which we based the stage definition.
- Are prior studies referenced appropriately?
The authors state that "with the exception of centrins and gamma tubulins" few canonical centrosome components are conserved in Plasmodium. These parasites are in fact able to assemble a more or less canonical centriole for microgamete basal body formation. Widely conserved centriolar components such as Sas6 are coded by the malaria genome, and have been characterized previously. This work is neither referenced nor discussed in the manuscript.
The reviewer is right to point out this omission. We were too much focussed on the blood stage centriolar plaques while writing this section, where centrioles are not observed. Of course centriole-like structures are relevant in other life cycle stages, such as microgametes, and should be discussed (line 104). Some previous attempts to endogenously tag Sas6 to verify its localization in blood stages were unfortunately not successful.
- Are the text and figures clear and accurate?
I find the timings shown in Figure 1A, with respect to the schematic quantification shown in Figure 1B, confusing. Shown as it is, one naturally correlates the images on Fig1A above with the cell cycle progression timing shown on Fig1B, below. However, by time 260min, for example, two somewhat adjacent centrin signals can be observed. Though this is defined as anaphase- by an unspecified criterium- this could very well be representative of metaphase. Nonetheless, the timing shown on Figure 1B for "anaphase" onset is 170min, which is inconsistent with the images above. I suggest that either, the quantification is shown in a different format (ex. bar plots) which could then better reflect the cell to cell variations observed (by use of error bars, for example) or that the figure explanation in the results section clarifies this issue.
We understand how this representation is misleading and have adjusted the figure and text accordingly. We modified the time stamps in Fig. 1A (now Fig. 1C) to the scale used in Fig. 1B (now Fig. 1D) i.e. collapse of the hemispindle is t=0 and explain this in the text (line 158). Since we feel that Fig. 1B (now Fig. 1D) is a good and compact visual representation of progression through the first division we kept the bar plots in the supplements (Fig. S1), but added a title clarifying that average duration between multiple movies are shown.
As presented, the data in Figure 1C is rather uninformative. A pattern could be more immediately extracted if dots corresponding to subsequent appearance of centrin dots in the same nucleus were connected to each other.
Concerning the appearance of the centrin signals we adopted the good suggestion by the reviewer and connected “paired” centrin signals by lines (Fig. 1E).
- Do you have suggestions that would help the authors improve the presentation of their data and conclusions?
There are a number of edits required on the text. Row numbers would have been helpful in pointing these out. I point some edits below, but thorough revision of the manuscript for grammatical and synthetic errors would be beneficial.
Cytokinetic segmeter - please replace with "segmented"
Please refer to Figure 1D when appropriate - there is quite an extensive paragraph describing the results shown on this figure, but it is only referenced at the start.
"..., as did the and the number of branches per nucleus,..." please rewrite as appropriate.
We apologize for not providing line numbers, but have corrected the addressed points and applied a grammatical check throughout the manuscript. We have added additional references to Figure 1D (now Fig. 2A) in the text.
Reviewer #1 (Significance (Required)):
This manuscript could be interested to a wide audience interested in cell cycle, cell division, cell organization and organelle positioning, infectious diseases and microscopy. However, the introduction assumes that readers are somewhat experts in the malaria field. I suggest the authors include a brief introduction of the malaria life cycle, and a schematic representation of the division mode. This will help non-experts follow the narrative more easily.
We are happy to read that the reviewer sees value of this study for a broader audience. Following the suggestion, we added a small schematic (Fig. 1A, lines 54, 62) highlighting the relevant steps of schizogony and expanded the introduction of the life cycle (line 46).
This work rectifies long-standing inconsistencies observed by different experimental approaches in the nuclear organization of malaria parasites during schizogony. However, what the functional consequences of the alternative modes of spindle organization in malaria could be, are not clearly stated or discussed. In this respect, as it stands, the manuscript is rather descriptive and lacks mechanistic insight. Nonetheless, the data presented are of superb quality, and the manuscript represents a tremendous leap in structural insight and imaging resolution for the field of malaria. I find the data is suitable for publication albeit minor adjustments are made (specially to Figure 1 and/or the description of the results shown in Figure 1, for consistency).
We agree that the value of this manuscript lies in the clarification of conflicting data, unprecedented structural insight, and providing a useful working model for the malaria parasite centrosome. Although this study is ultimately descriptive it forms the indispensable basis to generate more meaningful functional insight about centrosome biology and nuclear division. Some of the functional consequences worth considering are: i) The (at least) bipartite composition indicating that centrosome functionality is spatially spread throughout the nucleoplasm/cytoplasm boundary. ii) The delayed appearance of the centrin signal after tubulin signal allows the prediction that centrosome assembly is a staged process occurring over an elongated period of time. iii) The generally amorphous structure of the compartment predicts the involvement of yet to be uncovered matrix-like proteins harbouring microtubule nucleation sites. iv) Lastly, our model has important implications for the mechanism of centrosome duplication. In a centrosome containing centrioles (like in vertebrates), the duplication event can easily be explained by physical separation of the daughter and mother centrioles. Spindle pole body duplication in yeasts is achieved by de novo formation of a new one, which remains connected by a half bridge until it is split. The centriolar plaque organization revealed here suggests that we need an entirely new model of centrosome duplication (or splitting) to describe and understand this process in malaria parasites. We now address those points more explicitly in the discussion section (e.g. lines 375, 443, 467).
**Referee Cross-commenting**
I agree with all the other reviewer's comments. I'm glad the reviewers seem to be experts in the field of malaria cell division and have pointed out previous studies which were not appropriately referenced. I second those comments.
Reviewer #2 (Evidence, reproducibility and clarity (Required)):
**Summary:**
The manuscript by Simon et al have used advance cell biology technology like STED, expansion and live cell imaging to decipher the configuration of microtubules, centrin and nuclear pore during unconventional cell division process in malaria parasite. They have shown the dynamics of centrin and its localisation with respect to centriolar plaque that is characteristic of these parasite cell during schizogony> They also implicate from their studies that there is extended intranuclear compartment which is devoid of chromatin
**Major Comments**
Are the key conclusions convincing? Yes to some extent
Should the authors qualify some of their claims as preliminary or speculative, or remove them altogether?
*Some part are preliminary and speculative as there is no solid data supporting it. Please see below
- Would additional experiments be essential to support the claims of the paper? Request additional experiments only where necessary for the paper as it is, and do not ask authors to open new lines of experimentation.
*Yes to substantiate their claim
- Are the suggested experiments realistic in terms of time and resources? It would help if you could add an estimated cost and time investment for substantial experiments.
*They can do these quite quickly less than a month
- Are the data and the methods presented in such a way that they can be reproduced?
*Yes
- Are the experiments adequately replicated and statistical analysis adequate?
*Yes
The authors present beautiful imaging and some in depth structure using tomography and CLEM to show the location of centrin which is generally considered the marker for centrosome or Microtubule organising centre in malaria parasite. These approaches are still not been applied in Plasmodium and hence very informative. Though they present some advance microscopy but a lot of these concept for hemispindle were shown earlier in many light and super resolution microscopy studies. Authors claim that they are first to show that there is space between centrin and nucleus but it has been show previously in centrin studies in Plasmodium berghei using super resolution microscopy (Roques et al 2019 Fig1 and supplementary videos1&2) as well as expansion microscopy recently by group of Brochet etal 2021.
We thank the reviewer for the appreciation of our work. We are, indeed, not the first to describe the gap between centrin and tubulin or the nucleus. We just aimed to reiterate this finding, also visible in our data, in order to transition to the analysis of nuclear pore positioning to clarify whether centrin is actually extranuclear. Nevertheless, we should have cited the Roques and Bertiaux et al. studies again in this context, which we have now rectified (line 252).
In addition the microtubule dynamics was also recently shown with Kinesin5 live cell imaging for schizogony in Plasmodium berghei (PMID: 33154955) which author have omitted in their manuscript.
We thank the reviewer for pointing out the Kinesin-5 study by Zeeshan et al., which we failed to cite and discuss. We now state the findings of this publication and put it into the context of our work (see also answer to next point). Microtubule associated proteins, such as the microtubule plus end tracking EB1 and the aforementioned Kinesin-5, are indeed useful markers to investigate microtubule dynamics leading to the interesting results shown by Zeeshan et al. Nevertheless, we want to point out that labelling microtubule associated proteins (MAPs) remains an approximation of the underlying microtubule organization. As the authors in Zeeshan et al. indicate by themselves, Kinesin-5 does not decorate axonemal microtubules or the membrane-associated microtubule structure formed during cytokinesis in very late schizont stages. Further, colocalization between alpha-tubulin and kinesin-5 in schizont-stage parasites is not complete indicating a preferential decoration of certain sections of the microtubule structures (possibly the microtubule ends), which could only be resolved by super-resolution microscopy. Using a live cell dye, such as SPY555-tubulin, which directly binds to microtubules will provide a uniform labelling of any microtubule species and hopefully prove useful to the field in the future. Lastly, we present time-lapse microscopy analysis of blood stage cells, contrary to single time point images of live cells, providing a quantified chronology of microtubule reorganization at single cell level (with time stamps). Therefore, we feel that our claim, although it should be relativized, is formally speaking accurate.
It is also important that authors give valid discussion about previous studies on hemispindle, microtubule dynamics with respect to schizogony (PMID: 18693242; PMID: 11606229; PMID: 33154955) rather than giving the impression that they have given this concept first time on hemispindle dynamics and centrin location during schizogony.
We agree that those studies should be discussed in more detail. We are grateful to the reviewer for pointing out the Fowler et al. 2001 (PMID: 11606229) study. They use an antibody against gamma-tubulin to demonstrate its presence at the apical pole of subpellicular microtubules (f-MAST) in the merozoite and cytokinetic stages (line 102). However, we were unable to reveal a specific gamma-tubulin staining using the antibody used by them in the preceding schizont stage. After trying many different commercial gamma-tubulin antibodies and attempting to generate our own we now finally observe a gamma tubulin localization at the poles of intranuclear spindles in schizont stage, although the only successful antibody still displays some background staining, possibly including cross-reactivity with alpha or beta-tubulin (Fig. S4, line 237).
The highly insightful study by Mahajan et al. 2008 (PMID: 18693242) indeed suggests that centrin localizes away from the DNA and demonstrate the distinct localization from tubulin. They, however, likely due to the resolution limit of their microscopy techniques, speculate that the centrin signal is embedded in the membrane, while we could show by super-resolution and nuclear pore staining that centrin is distinct from the membrane (now Fig. 2A; line 257). The work done by Zeeshan et al. 2020 (PMID: 33154955) nicely shows dynamics of kinesin-5 in nuclear division. In schizont stages Kinesin-5 signal elongates and splits alongside the mitotic spindle with which it overlaps for the most part. Colocalization with centrin is less strong although the authors note some overlap. Our data suggest that centrin and tubulin are clearly distinct. In male gametes the authors show nicely time-resolved data of kinesin spreading along the elongating spindle, although hemispindles are not observed at this stage. We introduce and discuss these findings (lines 123, 432).
The concept of bipartite centrosome is already been discussed in Toxoplasma and the claim by authors in Plasmodium presented here is not substantiated experimentally. They showed that centrin is part of outer region while they do not show with any marker for the inner region. It will be very helpful if the authors use gamma tubulin or MORN1 to show the location with respect to centrin and microtubule. In the absence of this localisation the claims are preliminary and speculative. If the centrosomal protein complex is not involved in microtubule nucleation, then how the nucleation is happening. What are the molecules present in this amorphous matrix? It will be great to check the location of gamma-tubulin or some inner centrosome molecules described in Toxoplasma that is deemed to be MTOC.
We share the opinion that our Plasmodium data should be compared to Toxoplasma, while still being assessed independently. Despite Toxoplasma belonging to the apicomplexan the conclusion that their centrosomes should be organized in a similar fashion is by no means self-evident considering for example their significant evolutionary distance. Actually, several noteworthy morphological differences have already been well documented. i) Toxoplasma MTOC does contain centrioles in the outer core which is coherent with the centrin and gamma-tubulin localization in this region. ii) Toxoplasma MTOC contains an additional nuclear membrane protrusion enclosing the inner core. iii) mitotic microtubules in Toxoplasma are thought to penetrate the nuclear membrane to connect to centromeres. iv) the inner and the outer core are both extranuclear and therefore not to be equated with the intranuclear compartments. We now expand a bit on the discussion of the aforementioned differences (line 382). Nevertheless, we thank the reviewer for making us realize that the term “bipartite” is a poor choice to describe the centriolar plaque organization in this context. Therefore, we replaced it in the abstract (line 29) and the main text (line 375).
We acknowledge the fact that it would be desirable to show a marker localizing to the intranuclear compartment, and not only through visualizing the microtubule nucleation complex (Fig. 4A-B) and the positioning of the microtubule ends in this region (Fig. 3A). Concerning MORN1 we found no indication in the published localization data that it is, like in Toxoplasma, associated with the nucleus in Plasmodium species, where it is only found associated with the budding complex (and we are currently unable to procure an antibody) (line 422). We have attempted gamma-tubulin visualization on many occasions throughout the project (transgenic parasite lines, commercial antibodies, self-made antibodies) and only recently found an antibody revealing some specific signal. Indeed, we found localization at the poles of the spindles i.e. the intranuclear compartment (line 237). Unfortunately, this “best-possible staining” still showed some unspecific spindle staining likely resulting from cross-reactivity with alpha- or beta-tubulin causing us to put these data into the supplements (Fig. S4).
We had more luck with attempting a “new” type of staining, recently used in Plasmodium (Bertiaux & Balestra et al. 2021) using a fluorophore-coupled NHS-Ester in expanded samples. This chemical unspecifically stains proteins and revealed that the centrosomal region contains an exceptionally protein dense “hourglass-shaped” structure (Fig. 3F-H). Since the outer part of this structure colocalizes with centrin and the inner part overlaps with microtubules we assume that the centrosomal complex stretches throughout the nucleo-cytoplasmic boundary and fills part of the intranuclear compartment (line 320). Especially the highly protein dense region at the neck of the “hourglass” seems very coherent with the nuclear membrane embedded electron dense region which can be seen in electron microscopy (e.g. Fig. 3E & 4B). We feel that this staining strongly supports the presence of this novel intranuclear compartment.
The expansion microscopy is very nice and some of it presented in supplementary can be moved to main section.
Thanks for sharing our enthusiasm about this imaging technique. We have now selected a representative image of a hemispindle and mitotic spindle stage nucleus imaged by U-ExM and added it to the main section (Fig. 2B, line 231).
The localisation CenH3 is bit puzzling as it has been shown that centromere/ kinetochore cluster and are present during early and mid schizogony. The various foci with respect to nuclei are not what has been seen previously. Please discuss the difference in these two findings.
The localization pattern can easily be explained by the increased resolution of STED nanoscopy used in this study. Previous studies (e.g. Hoeijmakers et al. 2012 and Zeeshan et al. 2020) used classical confocal microscopy. Under those imaging conditions the individual foci seen here can´t be resolved and would, in accordance with the other studies, appear as one cluster. We slightly modified the text for more clarity (line 247).
Reviewer #2 (Significance (Required)):
- Describe the nature and significance of the advance (e.g. conceptual, technical, clinical) for the field.
* This is more technical advancement on the subject of centrin by using STED, tomography and CLEM.
- Place the work in the context of the existing literature (provide references, where appropriate).
* This work has relevance relation to cell division during schizogony in asexual stages in par with Toxoplasma or in Apicomplexa in general
- State what audience might be interested in and influenced by the reported findings.
Working with Apicomplexa, Protist, cell division and mitosis.
- Define your field of expertise with a few keywords to help the authors contextualize your point of view. Indicate if there are any parts of the paper that you do not have sufficient expertise to evaluate.
Working on Cell division in Plasmodium.
**Referee Cross-commenting**
I agree with the reviewers and some of the experiment suggested and the minor details have to be addressed. There are some loose ends and these suggestions will enhance clarity of the data. It is a very nice study and some of the comments suggested by reviewers will improve the manuscript. __
Reviewer #3 (Evidence, reproducibility and clarity (Required)):
**Summary:**
The centrosome is the primary microtubule-organizing center (MTOC) in eukaryotic cells that nucleate spindle microtubules necessary for chromosome segregation. In most eukaryotic cells, the canonical centrosome is composed of centrioles surrounded by an electron-dense proteinaceous matrix named the pericentriolar matrix (PCM) competent for microtubule nucleation mitotic spindle assembly. Following the breakdown of the nuclear envelope breakdowns, the mitotic spindle microtubules gain access to the kinetochores of the condensed mitotic chromosomes. Once the mitotic spindle is fully developed, centrosomes are at opposite poles of the cells, and chromosomes are pulled toward opposite poles. Cell division completes with cytokinesis resulting in the active formation of two nuclei within two daughter cells. Interestingly, during its asexual replication cycle, the malaria parasite Plasmodium falciparum undergoes multiple asynchronous rounds of mitosis with segregation of uncondensed chromosomes followed by nuclear division within an intact nuclear envelope. The multi-nucleated cell is then subjected to a single round of cytokinesis that produces dozen of daughter cells. We know about the Plasmodium centrosome is that it is made of an acentriolar structure embedded in the nuclear envelope and serves as MTOC during cell division. However, the biogenesis and regulation of the Plasmodium centrosome are poorly understood. Given the peculiarity of the cell division in Plasmodium parasites, understanding the molecular mechanisms that drive and regulate MTOC duplication and maturation could unveil novel targets for the treatment of malaria. In this study, Simon et al. successfully applied challenging and cutting-edge microscopy techniques to monitor the dynamic formation of the spindle microtubules and MTOC during Plasmodium intraerythrocytic mitosis. In addition, they remarkably combined stimulated emission depletion (STED) with ultrastructure expansion microscopy to define an uncharacterized intranuclear compartment devoid of chromatin as the nucleation site of nuclear microtubules. And lastly, the authors adapted an in-resin correlative light and electron microscopy (CLEM) approach to define the centriolar plaque position in a novel intranuclear compartment with centrosomal function.
**Major comments:**
In the methods section, it is stated that across this study, three different anti-tubulin antibodies (alpha-tubulin B-5-1-2, alpha-tubulin TAT1, beta-tubulin KMX1) were used, and two anti-centrin antibodies (TgCentrin1 and PfCentrin3) were used, one of which seems to have been generated in this study (anti-PfCentrin3). It is unclear in the figures or results section when each of these antibodies was used, and the authors should give a rationale for using multiple antibodies in combination.
To label microtubules we used the mouse anti-alpha-tubulin B-5-1-2 (Sigma, T5168) antibody throughout the study. Except for U-ExM were we added two additional primary antibodies against tubulin. Due to the expansion of the samples the antibody binding epitopes are stretched out in space. This causes a significant reduction of local epitope concentration (expansion factor 4.5 in all directions results in ~ 80-fold increase in the volume), which can reduce the signal intensity. Adding multiple antibodies binding different epitopes of tubulin can compensate for this dilution effect to some degree, as has been shown before by Gao et al. 2018. At the same time the expansion contributes to the accessibility of the usually densely packed tubulin epitopes within the microtubule polymer, which certainly adds to the success of U-ExM. What the respective contributions of those effects are is not clear, but we found superior signal-to-noise ratios when combining three tubulin antibodies instead of using one. The TgCentrin1 antibody was only used in Fig. 2C (now Fig. 3B) and validated the localization pattern of our new PfCentrin3 antibody we used in the other pictures. We now provide clearer description of antibody usage in the methods section and a new supplemental table.
The anti-PfCentrin3 antibody seems to have been generated for this study. If this is the case, the authors should provide evidence that this antibody binds to the recombinant PfCentrin3 it was raised against and binds PfCentrin3 in parasite lysates.
The anti-PfCentrin3 antibody was, indeed, produced for this study and we should have provided our western blot data right away. We now show the requested blot, which shows bands at the appropriate size in parasite lysate as well as for the recombinant protein, in the supplements (Fig. S2, line 178).
In the first paragraph of the Results section, the authors' remark of centrin foci that they are "...only detectable later (Mov. S2) or sometimes not at all." In Figure 1 A-C, it is implied that the first observed division is the first nuclear division of that parasite. Given that some nuclei do not have a visible centrin focus, it cannot be concluded with certainty that these parasites only contain a single nucleus and that this is their first division. The authors would need to include a quantifiable DNA stain to show this unequivocally to show a single nucleus. It has undergone DNA replication, similar to Klaus et al., 2021 BioRxiv paper. In the absence of a DNA stain, the authors should reword to clarify that this is the first observed division and speculate that it is the first division of that nucleus, but the authors should draw no firm conclusions about the first division.
Indeed the variability in protein levels that can result from exogenous expression can lead to some cells not showing clear Centrin1-GFP foci. Although this is a rare event we wanted to acknowledge this observation. The live cell microtubule staining using Spy555-Tubulin we use is, however, highly specific and sensitive and would stain any nucleus undergoing division including the first one. If there would be more than one nucleus in the observed cell it would unequivocally show two clearly separated tubulin signals (hemispindle or mitotic spindle). To illustrate this we added Fig. 1B (line 148) showing two live parasites stained with SPY555-Tubulin plus a Hoechst-based dye showing one or two nuclei alongside the corresponding tubulin signal. We modified the text to clarify how we stage the parasite for time-lapse acquisition (line 154). We already extensively experimented with state of the art fluorogenic live cell DNA dyes (e.g. from Spirochrome and the Johnsson group) to visualize the nuclei directly in time lapse microscopy, but even at minimal concentrations they all significantly inhibit mitotic progression. We also add this information in the main text (line 150).
In the first paragraph of the Results section, the authors write: " We quantified the duration of hemispindle, accumulation and anaphase stages ...." Anaphase spindle fibers means that the sister chromatids are separated. In the absence of a centromeric marker like NDC80, it doesn't seem easy to claim the anaphase stage. The authors should write " extended spindle." The authors might also consider using the term collapsed spindle instead of accumulation to reflect the dynamic of the intranuclear microtubules during the blood-stage replication. The same modification should be made for Figure 1B, so we read " hemispindle, collapsed spindle and extended spindle."
We thank the reviewer for this suggestion, which is very much in line with a comment by Reviewer 1 on the definition of anaphase. We acknowledge that the term is ill-defined here. Further, it suggest a mitotic morphology analogous to the one observed in “classical” models (prophase, metaphase, anaphase,…), which is not fully appropriate. Consequently, we decided to adapt the suggested terminology in Fig. 1 (and also new Fig. 2) and in the text (line 160).
Based on the evidence in this study, it cannot be stated unequivocally that the centrosome is entirely extranuclear, at least not as it is implied in Figure 3C. In Supplementary Figure 4, the microtubules appear to be extruding from a circular structure that may either be intranuclear or span the nuclear envelope. In Supplementary Figure 6, the structure pointed to as the centrosome appears to be embedded within the nuclear membrane with a top structure on the cytosolic side of the nuclear envelope. Thus, the best support for an extranuclear centrosome comes from the CLEM images. Still, it is noteworthy that the double membrane of the nuclear envelope is not visible on this slice in the region where the centrin fluorescence is found. Considering some of the fluorescence pixels for centrin are outside the parasite plasma membrane, and some of the Hoechst pixels are outside the nuclear envelope, this data does not show unequivocally that centrosomes are entirely extranuclear. However, this argument would be strengthened if the authors performed a proteinase K protection assay (or something similar) to determine if Centrin1 and Centrin3 are exposed to the cytosol. However, in the absence of that or further evidence, the authors should dampen their claims about the centrosome being exclusively extranuclear, as represented in the schematic in figure 3C.
We thank the reviewer for this comment, which highlights an issue in our communication of our working model of the centriolar plaque. At no point we intended to claim that the centrosome is exclusively extranuclear. Rather, centrins, which are currently the only reliable marker proteins, localize to a subcompartment of the extranuclear region of the centriolar plaque. Additionally, the centrosome clearly contains an intranuclear region. The composition of this intranuclear compartment is elusive, except that it harbors microtubule nucleation sites. Indeed, our model in Fig. 3C (now Fig. 4C) is misleading and not well annotated. The newly added NHS-Ester staining fortifies this claim (Fig. 3F-H. Consequently, we corrected our working model by adding an explicit figure labelling (now Fig. 4C).
We apologize for the misleading labelling in Fig. S6 (now Fig. S7). The green arrow was intended to point out the electron dense region associated with the nuclear membrane, which has been seen in previous studies, and was not intended to represent the entire extended centriolar plaque. If anything, this smaller region might provide the link between the intra and extranuclear compartments that the reviewer also identified in Suppl. Fig. 4 (now Fig. 2D). We modified the annotation of the Fig. S7 and Fig. 4A-B accordingly, labelling it the “electron dense region”. More importantly, we hope that our newly added data using NHS-Ester staining of protein dense regions (Fig. 3F-H) highlights the spread of the centrosome across the nucleo-/cytoplasmic boundary more clearly.
Considering whether centrin is actually extranuclear, we feel that the data shown in Fig. 2A (now 3A) is convincing. We have, however, added two panels of the relevant regions showing centrin localization respective to the nuclear pore and adjusted the contrast as we acknowledge the limited “visibility” within the unadjusted panels. The fact, that the centrin signal slightly overlaps with the nuclear envelope in CLEM images can be explained by the relatively poor resolution of the widefield microscope we had to use to image the sections. From the other super-resolution images in the manuscript, we know that the perimeter of the better resolved centrin signal is significantly smaller. Otherwise one had to assume from the CLEM data that centrin is also in the cytosol of the red blood cell and that DNA is localized outside the nucleus. On a similar note the fluorescence image is, contrary to the tomography image, a single slice since the thickness of the sample section (about 200nm) is significantly below the z-resolution (about 500nm) of a fluorescence microscope.
Throughout the study, the level of biological replication is unclear. The authors rigorously include all the data points for each of their graphs and the total number of images/videos quantified. And what needs to be added, in either the figure legends or a methods section, is the number of biological replicates for each of these measures came from.
We have added the number of replicas in the figure legends.
**Minor comments:**
STED is present as an acronym in the abstract and should be spelled out in full and clarified that it is a super-resolution microscopy technique.
We opted to remove STED from the abstract (leaving it at super-resolution, which includes expansion microscopy) to avoid disrupting the “flow” of the abstract and now spell out the acronym at the first mention in the introduction (line 127).
The second paragraph of the Results section states that ring and early trophozoite stage parasites do not express tubulin or centrin. Still, only an early trophozoite is shown in Supplementary Figure 2. Therefore, the authors should either include a similar image of a ring-stage parasite or remove ring-stage parasites from that statement.
We have removed the ring stages from the statement.
The second paragraph of the Results section contains the sentence, "At which point tubulin is reorganized into the bipolar microtubule array, which then forms the mitotic spindle cannot be resolved here." The authors are implying that the point at which tubulin is reorganized into the microtubule array, which goes on to form the mitotic spindle, cannot be resolved here. This is not particularly clear, though, and this sentence could be reworded for clarity.
We reformulated the sentence to clarify the point we failed to make with the previous wording (line 188).
The second paragraph of the Results section contains some statements about the results without referencing the figures that these statements come from. The authors should clarify this to make clear which figures each statement refers to.
We added more references to the appropriate figure throughout the paragraph (lines 188, 219, 223).
In the third paragraph of the introduction section, the authors write, " Centriolar plaques seem partially embedded in the nuclear membrane, but their positioning relative to the nuclear pore-like "fenestra" remains unclear." Unfortunately, the lack of reference did not allow me to understand if the authors state literature or comment on past published results.
We added the reference which was incorrectly positioned before the sentence instead of at the end (line 82).
the authors could add some references:
Second section of the introduction: " the 8-28 nuclei are packaged into individual daughter cells, called merozoites ( Rudlaff et al. 2019 PMID: 31097714)
Third section of the introduction: " The centrosome of P.falciparum is called centriolar plaque" ( Arnot et al. 2011, Sinden 1991a); " the nuclear pore-like "fenestra" remains unclear (Wall et al. 2018; Zeeshan et al. 2020).
Fourth section of the introduction: " tubulin antibody staining are extensive structures measuring around 2-4um ( Ref?)
When the authors introduce subpellicular microtubules of segmented schizonts, a reference to a study that shows these structures should be included.
A previous study that shows the distinct structure of microtubule minus ends should be cited when this structure is described.
Third section of the results, the authors should cite Bertiaux et al. 2021 with the Gambarotto et al. 2019 paper regarding U-ExM.
We apologize for missing some important references or putting them in the wrong position. We now added all the references or cite them again at the appropriate locations throughout the text.
Figure 1E shows hemispindle and mitotic spindle lengths of U-ExM expanded parasites, but the position within the figure and figure legend implies that these lengths were determined unexpanded parasites. Therefore, it should be stated in the figure legend that these measurements come from U-ExM expanded parasites. Moreover, I encourage the authors to include U-ExM images in the main figures. The images are beautiful, represent a significant technical achievement, and directly relate to Figure 1E. To the best of my knowledge, this is only the second study to perform expansion microscopy on Plasmodium and the first to use PFA-fixed parasites and a nuclear stain. It would be valuable for the Plasmodium and ExM communities to see this technical advancement represented in the main text.
We thank the reviewer for the appreciation of our ExM data and added it to Fig. 2B before the quantification of the microtubule length and number and added the information to the legend.
In the second paragraph of the Results section, the authors write, " but clearly display the microtubule cytoskeleton associated with the inner membrane complex." It would bring clarity to define in few words what the IMC is.
We included a short definition of the IMC (line 223).
The methods section details that the length of microtubules was determined by dividing the observed values by an expansion factor of 4.5. If the authors recorded the expansion factors of their gels, this data should be included, and how it was recorded should be stated in the methods. If not, the authors should include the rationale of using an expansion factor of 4.5 as this is slightly different from the previously published expansion factor of P. falciparum of 4.3.
We recorded the expansion factor by measuring the gel size pre and post expansion with a ruler and found a factor of 4.5 on average. We added this information in the methods (line 688).
There are several parasite lines used in this study, and some figures are not clear what parasite line was used. Could the authors please include the parasite lines in the figure legends of Figure 1 D-F, Figure 3, Supplementary Figures 1-2, and Supplementary Figures 4-7?
We added the parasite line information in the legends as requested.
Nuclear pore complexes, of which Nup313 is a component, can have cytoplasmic, integral, and nuclear-facing components. If it has been shown previously that PfNup313 is the homolog of Nup214 in vertebrates present on the cytosolic side of NPC, this should be stated. If not, then it should be clarified that it is unknown whether Nup313 faces the cytoplasm, nucleus, or is embedded in the NE, as this has implications for the colocalization of Nup313 and Centrin.
Nuclear pore proteins are very poorly conserved in P. falciparum and Nup313 has only been recently identified as such (Kehrer et al. 2018) mainly by the presence of FG-repeats (as for all the other newly defined proteins). The only related ortholog that can be found through BLAST search against humans, yeasts, and Arabidopsis is Nup100 from S. cerevisiae. ScNup100 is a central pore localizing protein but the sequence similarity to Nup313 is low. We are not aware of any findings showing relatedness to vertebrate Nup214, while sequence analysis rather indicates the absence of orthology. To clearly demonstrate the individual positioning of the few known Nups within the parasite´s nuclear pore complex would require a dedicated long-term project. However, due to the presence of FG-repeats one can assume that it is part of the central FG-Nups layer rather than of the intranuclear basket or the cytoplasmic filaments (line 255). Therefore it would localize more closely to the nuclear envelope than the latter. Either way, a clear gap between centrin and Nup313 signal can be identified and colocalization has not been observed. These data indicate that the exact position of Nup313 on the cytoplasmic, integral or nuclear-facing site is not decisive for the conclusions made in this study and our observations preclude scenarios where centrin is not extranuclear.
It seems from the image in Figure 2C that DRAQ5 and Hoechst have at least visually indistinguishable localizations. Have the authors taken any STED deconvolved images of nuclei stained with both Hoechst and DRAQ5? Considering the striking increase in detail of the Hoechst signal in STED deconvolved images, it may be informative both to this study and to people who work on chromatin organization what the chromatin staining looks like in the absence of bias towards chromatin state.
It would, indeed, be interesting to analyse chromatin organization by those means, but DRAQ5 is not a STED compatible dye, highly prone to bleaching, and therefore not suitable for such analysis. Being an infrared dye DRAQ5 is compared to the UV excited Hoechst also yielding a reduced spatial resolution, which is limited by the emitted wave length.
For the tomography and TEM images, the centrosome is indicated with an arrow, but it isn't entirely clear what that arrow is pointing to for some images. It would be clearer if the centrosome were outlined in green, like the NE, rather than just an arrow. This is particularly important for Supplementary Figure 4, where to my eye, it appears that the microtubules inside the chromatin-free region are coming directly out of a circular structure, which could be interpreted as the centriolar plaque.
The reviewer is right to point out the use of arrows for centrosome annotation. It was intended for orientation of readers to indicate the “likely position of the centriolar plaque” since a clear boundary around the centrosome can´t be defined. It would have been more precise to indicate that the arrow is pointing at the electron dense region associated with the nuclear membrane, which is of course only one of the sub-regions of the centrosome. This is particularly important since we want to emphasize the extended dimensions of the centrosome. Consequently, we modified the annotation to “electron dense region” in all concerned figures and corresponding legends.
The ordering of Figure 2A-C seems to imply that the DNA-free region was measured in the STED deconvolved images, but the methods imply that it was in the confocal images. The authors should clarify this in the figure legend or by rearranging B and C's order.
Hoechst signal was indeed acquired and measured in confocal mode and to avoid confusion we have changed the order of the figures (now Fig. 3B-C) as suggested.
The authors should provide some more detail on how the DNA-free zone was measured. For example, was it measured on single slices or maximum intensity projections? Was it measured from the middle, far, or near side of the centrin focus? Etc.
The measurement was carried out in the slice where the DNA-free zone was in focus. Depth was measured from below the centrin signal until the “bottom” of the DNA-free zone. We hoped that the little schematic above the figure would clarify this question, but acknowledge the need to more clearly explain the measurement method, which we now do in the corresponding figure legend (Fig. 3C).
The methods state that the mCherry signal in figure 2C was detected using a mCherry nanobody. This should be clarified in the figure legends as it currently seems as if we see endogenous mCherry fluorescence.
The visible signal is certainly a combination of the mCherry plus the “boosting” effect from the Atto594-coupled nanobody that we added. Clearly, this should be mentioned in the figure legend, which we now do.
The data in Supplementary Figure 4 seems vital to the interpretation of the study. Therefore, for clarity, I encourage the authors to include Supplementary Figure 4 in Figure 2.
We share the reviewers view on these data and moved them to the main figures (now Fig. 3D).
In the last sentence of the discussion, it is unclear what the authors mean by how the nuclear compartment "splits," could they please clarify?
We were referring to the event of centrosome duplication, which has to occur during nuclear division. In a structure without centrioles or a spindle pole body structure forming a half bridge we therefore need a new model to explain how the two poles of the spindle are formed. Potential modes are splitting or de novo assembly. This aspect, as also pointed out by other reviewer, warrants a bit more explanation, which can now be found in the discussion (line 468).
If the pArl-PfCentrin3-GFP plasmid or pDC2-cam-coCas9-U6.2-hDHFR have been published previously, the respective studies should be cited. If not, the study where the vector backbones were first established should be cited.
We have now cited the original studies publishing the vector backbones for the first time in the methods (lines 490, 501).
From the current text, it is not clear that the Nup313 tagged parasites also had a GlmS ribozyme. It is shown in Supplementary Figure 3, but the authors should clarify either in the text of the results, or figure legends, that this parasite line was Nup313_3xHA_GlmS
The Nup313-tagged line indeed has a glms ribozyme after the HA-tag, which we now mention in the figure legends.
In the plasmid constructs section of the methods, the authors list several primers by number but not by sequence. Instead, the authors should include the sequence and orientation of each of the primers mentioned in a table as supplementary data.
This is a good suggestion. We have generated a table at the end of the supplementary data file and on this occasion we also added tables of all the antibodies and dyes used in this study.
The authors should cite the study where the TgCentrin1 antibody was generated and provide the Rat anti-HA 3F10 antibody catalog number, as catalog numbers are provided for other commercial primary antibodies.
We now provide the missing catalog numbers in the supplemental data table.
There is an issue with the formatting of the journal-title in the Kukulski et al. reference.
Thank you for noticing this error, which we now corrected.
Reviewer #3 (Significance (Required)):
The genome of P. falciparum is fully sequenced; however, over 50% of encoded proteins are of unknown function, with many of these proteins unique to Plasmodium parasites. By identifying and characterizing essential biological processes, especially those divergent from human host cell processes, we will formulate ways to interfere with them by developing novel antimalarial drugs. The process of Plasmodium cell division differs from the classical cell cycle of its human host. In the study led by Caroline Simon, authors successfully utilized recent developments of super-resolution microscopies on expanded parasites to identify novel features of cell division machinery of the malaria blood-stage parasite.
Simon et al.'s work highlight the growing interest in the diversity of cell division mode of Apicomplexan parasites, which will likely contribute to a deeper understanding of the origin and functional role of the centrosome in eukaryotic life. In 2020, the Open Biology journal published a unique article collection named Focus on Centrosome Biology showcasing research that advanced our knowledge on centrosome function, evolution and abnormalities. In addition, the reported findings will interest research groups studying cell cycle regulation and evolution beyond the field of parasitology.
Our lab studies the peculiar cell cycle of Plasmodium falciparum to gain a functional understanding of mechanistic principles of nuclear envelope assembly and integrity during the cell division of the human malaria parasite.
**Referee Cross-commenting**
It is a wonderful study, and once all reviewer's comments are addressed, the manuscript should be in excellent shape for publication.
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scripting.com scripting.com
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My eyesight sucks, and if I'm not mistaken the screen isn't backlit
I had the very same problem with the #reMarkable. I really wanted to like it, but the missng backlight was a showstopper for me.
Now I take my handwritten notes on an iPad Pro 12.9, which is heavy with a less-than-great recharge cycle of one day.
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www.w3.org www.w3.org
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I'm partial to the "Principle of Least Power" in the Axioms of Web Architecture document cited in the bibliography. (The language there better captures the thought and presents it more convincingly, in my opinion.)
Shortcut: https://www.w3.org/DesignIssues/Principles.html#PLP
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www.reinsurancene.ws www.reinsurancene.ws
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According to reports from Keefe, Bruyette & Woods (KBW), industry executives are optimistic about the prospects for the run-off reinsurance market, which they say should benefit from rising pricing trends. KBW recently hosted a series of meetings with Florida and Bermuda re/insurance executives about their outlook on various sectors of the ... Read the full article
Industry execs optimistic about runoff, which should benefit from rising pricing trends.
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hypothes.is hypothes.is
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This appears to be evidence that one can (now) use emoji as tags in Hypothes.is?
It's the first time I've seen someone other than me make an attempt in the wild.
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- Jun 2021
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www.bz-berlin.de www.bz-berlin.de
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In den Häusern des Krankenhauskonzerns Vivantes gilt bereits seit Montag ein Besuchsverbot
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Für Geburten gilt künftig, dass sich die Frauen einen Menschen aussuchen dürfen, der sie begleitet.
§ 4 (1) S. 1 Krankenhaus-Covid-19-Verordnung
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Auch Seelsorge ist laut dem Papier weiter möglich.
§ 3 (3) S. 1 Krankenhaus-Covid-19-Verordnung
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Wegen des Wiederanstiegs der Corona-Neuinfektionen in Berlin sollen ab Samstag Besuchsregeln für die Krankenhäuser in der Stadt gelten.
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Menschen mit Symptomen, die auf Covid-19 hinweisen, dürfen laut der Verordnung allerdings nicht zu Besuch in Kliniken kommen.
§ 2 Krankenhaus-Covid-19-Verordnung
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Für den Besuch bei Schwerstkranken und Sterbenden sind keine Einschränkungen vorgesehen.
§ 3 (2) Krankenhaus-Covid-19-Verordnung
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Einmal am Tag sollen Patienten demnach von einer Person Besuch bekommen können – für eine Stunde.
§ 3 (1) Krankenhaus-Covid-19-Verordnung
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www.biorxiv.org www.biorxiv.org
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Reviewer #2 (Public Review):
The study sets out to answer what are the tissue specific mechanisms in fat and muscle regulated by the transcription factor E2F are central to organismal function. The study also tries to address which of these roles of E2F are cell intrinsic and which of these mechanisms are systemic. The authors look into the mechanisms of E2F/Dp through knockdown experiments in both the fat body* (see weakness) and muscle of drosophila. They identify that muscle E2F contributes to fat body development but fat body KD of E2F does not affect muscle function. To then dissect the cause of adult lethality in flies, the authors proteomic and metabolomic profiling of fat and muscle to gain insights. While in the muscle, the cause seems to be an as of yet undetermined systemic change , the authors do conclude that adult lethality in fat body specific Dp knockdown is the result of decrease trehalose in the hemolymph and defects in lipid production in these flies. The authors then test this model by presenting fat body specific Dp knockdown flies with high sugar diet and showing adult survival is rescued. This study concurs with and adds to the emerging idea from human studies that E2F/Dp is critical for more than just its role in the cell-cycle and functions as a metabolic regulator in a tissue-specific manner. This study will be of interest to scientists studying inter-organ communication between muscle and fat.
The conclusions of this paper are partially supported by data. The weaknesses can be mitigated by specific experiments and will likely bolster conclusions.
1) This study relies heavily on the tissue specificity of the Gal4 drivers to study fat-muscle communication by E2F. The authors have convincingly confirmed that the cg-Gal4 driver is never turned on in the muscle and vice versa for Dmef2-Gal4. However, the cg-Gal4 driver itself is capable of turning on expression in the fat body cells and is also highly expressed in hemocytes (macrophage-like cells in flies). In fact, cg-Gal4 is used in numerous studies e.g.:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4125153/ to study the hemocytes and fat in combination. Hence, it is difficult to assess what contribution hemocytes provide to the conclusions for fat-muscle communication. To mitigate this, the authors could test whether Lpp-Gal4>Dp-RNAi (Lpp-Gal4 drives expression exclusively in fat body in all stages) or use ppl-Gal4 (which is expressed in the fat, gut, and brain) but is a weaker driver than cg. It would be good if they could replicate their findings in a subset of experiments performed in Figure 1-4.
2) The authors perform a proteomics analysis on both fat body and muscle of control or the respective tissue specific knockdown of Dp. However, the authors denote technical limitations to procuring enough third instar larval muscle to perform proteomics and instead use thoracic muscles of the pharate pupa. While the technical limitations are understandable, this does raise a concern of comparing fat body and muscle proteomics at two distinct stages of fly development and likely contributes to differences seen in the proteomics data. This may impact the conclusions of this paper. It would be important to note this caveat of not being able to compare across these different developmental stage datasets.
3) The authors show that the E2F signaling in the muscle controls whether binucleate fat body nuclei appear. In other words, is the endocycling process in fat body affected if muscle E2F function is impaired. However, they conclude that imparing E2F function in fat does not affect muscle. While muscle organization seems fine, it does appear that nuclear levels of Dp are higher in muscles during fat specific knock-down of Dp (Figure 1A, column 2 row 3, for cg>Dp-RNAi). Also there is an increase in muscle area when fat body E2F function is impaired. This change is also reflected in the quantification of DLM area in Figure 1B. But the authors don't say much about elevated Dp levels in muscle or increased DLM area of Fat specific Dp KD. Would the authors not expect Dp staining in muscle to be normal and similar to mCherry-RNAi control in Cg>dpRNAi? The authors could consider discussing and contextualizing this as opposed to making a broad statement regarding muscle function all being normal. Perhaps muscle function may be different, perhaps better when E2F function in fat is impaired.
4) In lines 376-380, the authors make the argument that muscle-specific knockdown can impair the ability of the fat body to regulate storage, but evidence for this is not robust. While the authors refer to a decrease in lipid droplet size in figure S4E this is not a statistically significant decrease. In order to make this case, the authors would want to consider performing a triglyceride (TAG) assay, which is routinely performed in flies.
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github.com github.com
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All Bee v1.0 versions are incompatible with the v0.6 Swarm. Node operators who currently run nodes on the Swarm test network should not update to this version. This version is currently only rolled-out to the Swarm mainnet, to which node operators can operate fully-functional nodes when the BZZ token is circulating (after June 21st).
该版本同测试网的不兼容，到6月21日上主网了才能用。需要BZZ代币。
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www.adamhyde.net www.adamhyde.net
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Software is a conversation after all!
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- May 2021
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www.biorxiv.org www.biorxiv.org
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Note: This preprint has been reviewed by subject experts for Review Commons. Content has not been altered except for formatting.
Learn more at Review Commons
Referee #1
Evidence, reproducibility and clarity
Summary:
In the manuscript „Intra-helical salt bridge contribution to membrane protein insertion" the authors investigate the effect of salt bridge formation between positively and negatively charged amino acids on the insertion behavior of α-helical protein segments into the membrane. Generally it is believed that polar or even charged residues prevent stable membrane insertion of α-helical protein segments, but some of these authors had already shown in a previous paper that such residues are more frequent than expected in transmembrane helices. In the current study, the authors investigate in detail the role of intra-helical salt bridge formation on stable membrane insertion. Using an in vitro membrane insertion assay based on the E. coli leader peptidase (Lep) protein, they found better membrane insertion for helical segments with opposite charge pairs placed at positions compatible with intra-helical salt bridge formation (positions i→i+1; i→i+3 and i→i+4). Furthermore, the authors performed a database screen which revealed that oppositely charged residues are overrepresented at these positions. Finally they picked two candidate membrane proteins from the database (Halorhodopsin and calcium ATPase 1) and proved the presence of an intra-helical salt bridge and determined the contribution of the salt bridge to the apparent free energy of membrane insertion (ΔGapp), which was in the range of 0,5-0,7 kcal/mol.
Major comments
- It seems that the data in Fig. 3b has been mixed up, making it difficult to judge the conclusions. The bars with forward slash seem to represent the "same charge" data and the bars with backward slash seem to represent the "opposite charge" data (exactly contrary to the figure legend). In general the forward and backward slash representation is not easily distinguishable, and for the position i+4 both bars contain a forward slash (making it impossible to discriminate same and opposite charge). Please use filled and unfilled bars instead. Furthermore the bar diagram in Fig. 3a is stacked for opposite and same charge, whereas in Fig. 3b the respective bars are placed next to each other. Additionally the label of the y-axis in Fig. 3c is misleading, as it is not the "Frac. of opp. charged pairs" but the fraction of oppositely charged pairs that form salt bridges.
- The authors don´t give details no how the log odds ratios and the respective p-values have been determined. Please include this in the Materials and Methods section. What does a p-value of 0.00e+00 mean (see Table 2, Spacing: +3, "All Log odds")?
- What is the proof that for the isolated helix A from the calcium ATPase 1 the membrane embedded part is identical to the full-length protein? The authors investigated two different helix A peptides, the full-length helix ranging from L49-F78, and one short fragment ranging from L49-A69 containing the more hydrophilic N-terminal region, which is the membrane-embedded region in the full-length protein. The authors state: "In contrast, when only the membrane-embedded sequence was included, the Lep chimera was mainly doubly-glycosylated (Fig. 5c, lane 3), suggesting that helix A is properly inserted when the full helical sequence is present." In my opinion this conclusion cannot be drawn from the data presented. The authors used an isolated helical segment, so in my opinion it is much more likely that the isolated full-length helix inserted via its hydrophobic C-terminal part (L60-F78) into the membrane. The authors themselves state in their manuscript: "It has been previously shown that the position in the membrane of TM helices in protein folded structures does not always correspond to the thermodynamically favored positions in the membrane of the isolated helices." Also the i→i+5 mutant points into that direction, because the effect of disturbing the intra-helical salt bridge for the helix A is much less pronounced compared to the similar data in Fig. 4f for the Halorhodopsin protein. In my opinion this shows that most probably only one charged residue (R63) is embedded inside the membrane (with a membrane embedded part of L60-F78).
Minor comments:
- line 151: ",see Figure 2)" Typo: Bracket missing.
- line 172: "Other known structural features can also be hinted at, including aromatic ring stacking by His-Trp pair [20] at i→i+6." Please give some more examples of important structural features of membrane proteins, which can be seen in your analysis (e.g. I think that also the glycine zipper can be seen in the i→i+4 data set).
- line 255: "The salt bridge contributes approximately ~0,5 kcal/mol to the apparent experimental free energy of membrane insertion." Please explain that this value was derived from the comparison of the ΔGexp between the wt and the i→i+5 mutant. Please comment also on the large difference between the predicted (ΔGpred) and the experimental values (ΔGexp), even if no salt-bridge is involved (e.g. for the DD mutant).
- line 348: "Asp-Lys pairs at position i, i+4 and Glu-Lys pairs at position i→ i+3 are the most prevalent as seen previously in Figure 2. They are both among the most prevalent oppositely charged pairs and the charged pairs that form the highest number of salt bridges in membrane protein structures. This is in stark contrast to Glu-Arg pair at position i→ i+1 that although as frequent in pairs as Asp-Lys and Glu-Lys at positions i→i+4 and i→i+3 respectively, only form salt bridges in one-fourth of the cases." Fig. 2 shows that each charge pair has a different prevalence depending on the order (e.g. Asp-Lys and Lys-Asp pairs). I think for this statement the sum of both prevalences should be taken into account, and as the sum is not easy discernible from Fig. 2, it would help to include a table containing the sums. Furthermore, it would be good to refer also to Fig. 3, which also contains a part of the discussed data.
- line 402: "c-myc tag (Glu-Gln-Lys-Leu-Ile-Ser-Glu-Glu-Asp-Leu, EQKLISEEDL) was added in Ct in hanging with de PCR primer before cloning." Please revise the sentence and I think the one letter code for the c-myc tag is sufficient (please correct this also in line 428).
- line 420: "A region's total ΔG is the sum of these individual scores weighted on where in the region the residue, a residue in the middle of the helix has a higher weight than residues at the ends." Please revise the sentence, the meaning is unclear.
- line 436: "Total protein was quantified and equal amounts of protein submitted to Endo H treatment or mock-treated, followed by SDS-PAGE analysis and transferred into a PVDF transfer membrane (ThermoFisher Scientific)." Please revise the sentence.
- line 498: "Topological files with sequence and membrane topology are created with the help of the RCSB secondary structure file and only membranes annotated as pure α-helices were retained." I assume that the description contains a typo (membranes annotated as pure α-helices?)
- line 507: typo "..., but we did not clustered the proteins" 14: line 560: "The individual value of each experiment in represented by a solid dot being represented as a green square the experimental ΔG value for the L4/A15 sequence from [2]." Please revise the sentence. 15: line 562: "The wt and simple mutants are shown in white bars." Typo: single mutants 16: line 563: "Charges at compatible distances with salt bridge formation (i→i+1; i→i+3; and i→i+4) are shown in yellow. Not compatible distances with salt bridge formation (i→i+2; and i→i+5) are shown in dark gray. Compatible distances but not compatible amino acid pair (i, i+4 DD pair) is shown in clear gray." The given colors don´t match with the figure (i→i+1 = brown; i→i+3 = orange; i→i+4 = yellow and i→i+4 DD pair = white) 17: line 597: "The different monomers are shown in transparent blue, purple and indigo." The different colors are hardly distinguishable in the figure. 18: Figure 4a: The table could be simplified. I think the column "charges" can be removed, as it contains not really charges and the names of the peptides already contain the same information. The column "Å" contains only a value for the wt (and not for the DK i,i+5 mutant) and as the distance for the wt is also given in Fig. 4g, this column can be also removed.
- Fig. 4f: The marker lane is hardly visible (completely dark lane)
- Fig. 5b: The column "Å" contains only values for the wt sequences (long and short). See also comment 18.
- Fig 5d: Why is in the SDS gel a mass shift between the wt and the i→i+5 mutant visible, even though the peptide mass is equal.
- There are several changes of font type or format changes (e.g. line 210-214). Please correct this.
Significance
As a structural biologist with a focus on membrane-proteins, I understand that the study is concerned on intra-helical salt bridges, but the implications of inter-helical salt bridges should also be discussed, at least in the introduction or outlook. The authors propose that their results are important for the improvement of membrane protein topology prediction methods, so for this aim it is also necessary to take any potential inter-helical salt bridges into account. In this context, it would be relevant to point point out that there even exist extended rows of salt bridges between transmembrane segments (charge-zippers), which serve an important structural element in several membrane proteins.
The article is well written and most of the conclusions drawn from the experimental results are convincing. I agree with the authors that their results are relevant for future improvement of membrane protein topology prediction software, which so far does not take the possibility of salt bridge formation into account. Therefore, I recommend publication after clarification/revision of the abovementioned points.
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www.makeuseof.com www.makeuseof.com
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What Is Half-Duplex And Full-Duplex Operation, And How Does It Affect Your Router? By Phoon YS Published Sep 22, 2014 Share Share Tweet Email WiFi connections are running at half-duplex while the wired part of the LAN are on full-duplex. So it seems that by connecting through WiFi, something had to give. Were we shortchanged?
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- Apr 2021
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comicsandthecanon.wordpress.com comicsandthecanon.wordpress.com
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ideological dichotomy
This is defined as a sharp division of things or ideas into two contradictory parts.
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“It’s a lot easier to pull yourself up by your bootstraps, Mr. Man, if you already know how to fly!”
One can draw parallels to DuBois telling Washington that he would be considered privileged due to the fcat that he can be considered part of the "Top Tenth" because of his education and connections.
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When you can fly, there’s no burden you can’t bear. When you can fly, gravity can’t touch you. When you can fly, you can do anything”.
This reminds me of the ongoing metaphor in "Jubilee" of the slaves being cage birds. So with Augustus him having education, him being a free man, it gives him the ability to fly like a bird. Much like the age old saying the "the skies the limit".
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It limits the complexity and the roundedness of the characters
Like he said there is not room to build a character, to have a struggle to have redemption arcs, because they are just meant to be a symbol because of the limited representation
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the reverberations of the 1992 Los Angeles riots
The 1992 LA riots were caused because the LAPD had used excessive force in the arrest and beating of Rodney King, because of media it spread like wildfire.
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Dr. Martin Luther King Jr. and Malcolm X, and Ta-Nehisi Coates and Cornel West, to Nas and Jay-Z and Cam Newton and Colin Kaepernick
These are all prominent black men, from social activists, to philosophers, to rappers and athletes.
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ignorant and inexperienced
Perhaps this could be because of the fact he was born into slavery which is why he tends to lean more on realism and not idealism much like DuBois
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the contamination and death of the worst.
What did DuBois mean by this, what could be the contamination be? Maybe the struggle the rest of black Americans had to face in society
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“Talented Tenth.”
Its name is talented tenth because it is referencing the able ten percent of black Americans that developed leadership capacity from higher education
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Du Bois was a proponent of liberal arts education and argued for full civil rights for Black people
This is why DuBois had become one of Washington's biggest opponents because he did not believe in a "sitting duck" method, wanting to create change not waiting to be accepted.
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the South that the Negro is given a man’s chance in the commercial world
This is reminding me after the emancipation proclamation and after the civil war when the south was in a time of reconstruction, they had given freed slaves the ability to have land in the Midwest and begin their agricultural journey. Could this be in reference?
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Washington contended that the rights and privileges of true citizenship for Black people could only be gained through gradual struggle and the development of marketable skills.
I see Washington's philosophy as a form of assimilation and conformity to American society and to gradually comfort those with a negative view of black people.
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Educator Booker T. Washington was born into the institution of American chattel slavery.
This plays a role in why Washington's philosophy is what it is
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The ideological dichotomy
This just meaning the system of division of black and white Americans that many believed (and still do) believe in
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“The Negro Problem,”
This being to fix the societal gap between black people and white people
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“The Talented Tenth,”
The Talented Tenth is a term that designated a leadership class of African descendant Americans in the early 20th century
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Washington emphasizes the importance of achieving Black prosperity
He urged blacks to accept discrimination for the time being and concentrate on elevating themselves through hard work and material prosperity
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changing his identity to be the son, grandson, and great-grandson of Augustus Freeman I.
Represents how racial injustice continued throughout several generations just taking on various forms and altercations as time passed.
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a Black man who seeks to destroy the organization he once supported after he realizes their supposed Black outreach is actually a form of Black subjugation,
Somewhat represents the idea of double-consciousness and even Washington, when he funded Jim Crow opposing organizations and Black newspapers.
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Martin Luther King Jr. and Malcolm X
2 other figures with differing views but within the civil rights movement period. MLK advocated for confrontational and peaceful protests such as marches, boycotts, and sit-ins, while Malcom X promoted more violent approaches such as riots.
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While “The Atlanta Compromise” doesn’t directly critique Du Bois, Du Bois’s response deliberately excoriates Booker T. Washington’s stance.
Just as the poem we had to annotate as well, Washington speaks his views first, and Du Bois follows with his rebuttal.
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He deemed agitation and civil unrest for the sake of social equality to be “the extremest [sic] folly,”
Since Washington was born a slave, it's easier to understand why he has such views. He was born into an oppressive system and may not see a light at the end of the tunnel that Du Bois saw in which protesting for reform would bring him closer to.
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higher education
One of the common grounds shared between Washington and Du Bois, both were highly-educated individuals.
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a co-founder of the National Association for the Advancement of Colored People.
My Harlem Renaissance figure, Ida B. Wells, was also a founder of the NAACP.
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“The Atlanta Compromise,”
Washington was tasked with the objective to publicly speak to a majority-white crowd upon race relations and justice.
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Educator Booker T. Washington was born into the institution of American chattel slavery.
Washington was born into slavery, which Du Bois was not. This differing factor could contribute to their differing views concerning the strive for racial equality.
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The debate over the best sociopolitical direction for African Americans not only crosses over to different generations but also crosses over to different forms of media.
Refers to the various approaches to obtain racial equality presented from 2 different advocates. This problem has spread over generations and media outlets upon national coverage.
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in doing so often found many of their solutions standing in stark contrast to the ideas of their fellow Black intellectuals and activists.
Introduction to the differing ideologies between activists Washington and Du Bois
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Freeman initially turns down Raquel’s request, and suggests that she and the other Black people of Dakota should pull themselves up by their own bootstraps, to which Raquel replies, “It’s a lot easier to pull yourself up by your bootstraps, Mr. Man, if you already know how to fly!”
I personally think this is commentary on white privilege. Freeman doesn't see how difficult it is for Raquel, because he is born with a privilege that Raquel doesn't have.
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Augustus ages far slower than humans, allowing him to have lived through many major moments in American history
This gives the writer an opportunity to talk about different events that have effected the black community.
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“Golden Age” of hip-hop combined with the reverberations of the 1992 Los Angeles riots to create an atmosphere of interracial conflict, cultural celebration, and sociopolitical tension
Black culture became more and more a part of American culture. The social movements highly influenced American culture.
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His belief in access to liberal arts higher education stemmed from a belief in the potential for the Black intellectual elite to lead the race to prosperity and equality.
More education would mean more opportunities for black people to get involved in politics and law discussions.
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“W.E.B.” Du Bois once supported Washington’s sociopolitical approach before becoming one of its, and his, strongest and loudest opponents
This shows how as people do more research and look from different perspectives, their way of thinking can change.
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rather than seek access and opportunity through protest and civil unrest:
It has been shown in history time and time again that the only way to get equal opportunities and rights is through protest, unrest, and fighting back.
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Washington contended that the rights and privileges of true citizenship for Black people could only be gained through gradual struggle and the development of marketable skills.
He believed that in order for white people to get on the bandwagon of giving black people rights, they had to prove their effect on the economy.
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sociopolitical ideology and set of educational aspirations are best for the collective African American population.
He gave a new way of looking and thinking about this discourse.
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most notable rendering of the debate between Booker T. Washington and W.E.B. Du Bois is in Milestone Media’s Icon written by Dwayne McDuffie and illustrated by MD Bright.
Uses a different type of medium to confront the discourse between these two leaders.
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Booker T. Washington and Du Bois respectively.
They had very different ideas of how to solve the racial issues in America.
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solutions standing in stark contrast to the ideas of their fellow Black intellectuals and activists.
There were many ways Black Activists went about trying to fix this problem. Such as accommodating, fighting for equal rights, or just straight up leaving.
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Generations of Black writers and thinkers have taken to the task of solving what was coined “The Negro Problem,”
The Negro Problem refers to the separation of Black People from American Culture.
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The Negro Race, like all races, is going to be saved by its exceptional men. The problem of education then, among Negroes, must first of all deal with the “Talented Tenth.”
Educating the best minds of the race disseminates into the rest, allowing the general uplift of all.
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The Negro Problem
It covers law, education, disenfranchisement, and Black Americans' place in American society.
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Raquel’s youthful perspective most often wins over Augustus whose once-immutable opinions are made malleable after learning more about the current condition of Black people in Dakota.
Just like in irl, Raquel just like Dubois wins over people when faced with the truth concerning the problems of always abiding and assimilating in society.
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Icon provides a take on the generations-old debate that incorporates a popular medium the blends prose with sequential art.
It incorporates the debates between Booker and Dubois but to a more modern audience to interpret
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Raquel’s final words are enough to change Augustus’s mind, and he agrees to their becoming Icon and Rocket.
This shows the shift in ideas as Dubois Ideas became the center part for a lot of other black activist that came after him, such as MLK and Malcolm X
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underground railroad during slavery, fights for the Union in the Civil War, graduates from Fisk University during Reconstruction, lives in Harlem during the Renaissance, becomes an expatriate in France in the 1930s, and fights with the Allies is WWII.
This in context helps young black kids understand the history with African involvement in America
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. Unlike Superman, whose similar origin puts him in the present-day Kansas farm of two loving white parents, the Milestone alien crash lands on a southern plantation in 1839.
Contrast both characters as Superman landed in a happy time without any conflict in Kansas, while In Milestone, Icon lands in a southern planation where the brutal reality of slavery is taking place and mistreatment of blacks is the norm.
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music, politics, and energy of its time and indefatigably dedicated to authentic depictions of Blackness.
Show that young black people can relate to characters with their culture and be able to see themselves with what they might not always get with other super heroes.
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increasing authentic representation of people of color
At the time many of the times most famous pronounced super heroes were all white. With Captain America, Superman, and Batman to name a few.
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It limits the complexity and the roundedness of the characters.
That solely writing a character to depict blacks also does no justice to the character as it makes the character bland, so therefore why he creates characters with complexity and with the character being black, it helps the black community in the long run as it does not show stereotypes nor have a white washing effect.
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Hughes’s essay delivers a lesson
To teach that the black community can do anything no matter there skin religion and or gender
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monolithic depiction of Black people and Black culture
Monolithic meaning not open to new ideas and remaining with the same old stereotypes and depictions of blacks in the past.
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With a focus on increasing authentic representation of people of color, Milestone Media created a world of splash pages and panels that is both inextricably bound to the music, politics, and energy of its time—much like the Black Arts Movement
This site is here to help the Black community get more involved in poetry and music and other jobs that we may think only white people run
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“My problem—and I’ll speak as a writer now—with writing a black character in either the Marvel or DC universe is that he is not a man. He is a symbol. Like Wonder Woman—if you write Wonder Woman, she is all women
I agree with this not a lot of people go out and say my favorite hero is Wonder woman or my favorite hero is Black panther. I think we need more male black hero's
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felt the paucity of characters of color, queer characters, and women characters within American comics needed to be addressed
We need more hero's that are of different origin's I know of a few hero's that are black (Black Panther, Storm, and cyborg just to name a few.
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characters of color, queer characters, and women characters within American comics needed to be addressed.
All of these things being prevalent as there was still issues with women rights, gays being shamed , and blacks still being discriminated and stereotyped.
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Black artist downtown became more and more isolated from that so-called ‘mainstream’ by the growing need to fully express [their] soul and mind connection with Black struggle in [their] art and in the street”.
Shows me that black artists are dying down which isn't a good thing
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Cam Newton and Colin Kaepernick
Here I see Cam Newton abiding by the NFL therefore assimilating to the white audience, while I see Colin Kaepernick using his freedom of speech to voice his opinions on black lives
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Martin Luther King Jr. and Malcolm X
MLK taking the civil approach with civil protest, and Malcom X taking the violent riot approach of demanding rights now
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If white people are pleased we are glad.
To me you shouldn't do something just to please someone do it because you like to do it
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confines of society.
What I don't get is that if he came from a child hood where he was a slave and saw the impossible happen being the freedom of slaves, why not continue the ambitions of the slaves but instead continue to fight for their right stop be actually equal instead of being free, but confined by white society.
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Be stereotyped, don’t go too far, don’t shatter our illusions about you, don’t amuse us too seriously. We will pay you,’ say the whites.”
Shows me that the whites don't understand where this young poet is coming from and now yawl want to be nice to him just doesn't make sense
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lack race should be to obtain marketable skills within the current confines of society.
I can see why Booker T says this because after all he was a slave, when coming from an upbringing like that, all anybody would want is to just live life like how society already is instead of giving in for hope for change that might never come.
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The Negro artist works against an undertow of sharp criticism and misunderstanding from his own group and unintentional bribes from the whites.
People are gonna hate you for what you do and that's the truth I make music and not everyone likes it but I'm still standing tall
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higher education
Ironic how Booker T was the first one to set up a school for high education, which eventually led to Dubois getting his education and being Booker T biggest opponents.
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no great poet has ever been afraid of being himself
This is true through everything like being a song writer don't be someone your not just because a certain crowd doesn't follow you be yourself and your time will come
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the young poet tells Hughes that he wants to be “a poet—not a Negro poet,” which Hughes takes to mean that, at best, the young poet seeks to downplay his race
This shows me that this young poet doesn't believe in his race it shows me he is less confident about his race.
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founded for the higher education of African Americans.
He wants blacks to accommodate yet founded a school for high education for African Americans, that clearly goes against what many whites think of about black people. In my opinion contradicts his own statement.
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After emancipation
The order that gave freedom to slaves in 10 states during the civil war.
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provided them rather than seek access and opportunity through protest and civil unrest:
This is where I would disagree with him, as not seeking for opportunity in itself is already bad advice as given an opportunity one should take it.
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A proponent of vocational education for Blacks, Washington contended that the rights and privileges of true citizenship for Black people could only be gained through gradual struggle and the development of marketable skills.
This proves how Booker T Washington was living a double consciences, by living his life out but also pertaining to his white counterparts.
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over-century-old discourse
pre civil war and post civil war
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The debate over the best sociopolitical direction for African Americans not only crosses over to different generations but also crosses over to different forms of media.
This pertains with the many different activist with all differing views from one another
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civil disobedience
With Civil disobedience I think of Martin Luther King
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reactive aggression
Malcolm X
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isolation
This being Dubois
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assimilation
This being Booker T. Washington idea
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in doing so often found many of their solutions standing in stark contrast to the ideas of their fellow Black intellectuals and activists.
The disputes between ideologies, such as Dubois and Booker T, with Dubois arguing for having his rights and equality now VS Booker wanting to accommodate.
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hypothes.is hypothes.is
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I'm using this tag fo keep notes about the changes that need to be made now that Writefreely exists in its own organization on GitHub. See https://discuss.write.as/t/moving-the-writefreely-repo-on-github/2568
Tags
Annotators
URL
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hypothes.is hypothes.is
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All set up and ready to go.
welcome
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stackoverflow.com stackoverflow.com
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Which HTML tag I should use to enclose such notes to add a semantic meaning of a note that may be useful to read at a given point of a tutorial, but is not part of the main tutorial flow?
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A better description is in the specification itself. Why read secondary remarks when the source is written so good?
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I respectfully disagree with your assessment. You are referencing the quote "It's not appropriate to use the aside element just for parentheticals, since those are part of the main flow of the document." However the OP specifically said that they are looking for a semantic element for "a note that may be useful to read at a given point of a tutorial, but is not part of the main tutorial flow". That is what "aside" is for. It's not part of the main content flow.
That's a tough one. I can see it both ways.
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An admonition is a parenthetical
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<aside> is appropriate if the side note "could be considered separate from the content"
From a programmer's perspective:
- It shouldn't be in an <aside>, if it is actually directly about what is in <main>
- An <aside> should be able to be evaluated on its own, (almost entirely) in isolation from, and not dependent on anything in, the <main> content. This could be especially important/relevant for screen readers.
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<aside> is not appropriate if the side note is "a parenthetical". The W3C gives no examples of what it means.
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In my opinion, the W3C definition is unnecessarily confusing and restrictive. The dictionary definition of aside is "a temporary departure from a main theme or topic", and the spec should just stick to that, rather than introducing subtle distinctions.
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I believe the accepted answer is not quite correct. According to the HTML5 working draft, the <aside> element can be used to mark up side notes in certain, but not all cases:
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Of course, there is no reason why you can't use <aside> for all sidenotes, if it makes your code simpler. Think of it as civil disobedience. :)
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The dictionary definition of aside is "a temporary departure from a main theme or topic"
Tags
- everyone has different interpretation
- sidenote
- semantic meaning
- relationship: is a
- clarification
- I agree
- definition
- controversial
- unnecessarily restrictive
- good question
- aside
- makes sense to me
- subtle distinction
- definition/description
- tangentially related content (aside)
- you can do whatever you want
- why _ when _?
- open to interpretation
- respectfully disagree
- confusing
- prefer primary source over secondary source
- HTML: <aside>
- parenthetical
- appropriateness
- ambiguous
- use what works for you
- civil disobedience
- admonition
- semantic markup
- subjective
- I have this question too
Annotators
URL
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- Mar 2021
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book.douban.com book.douban.com书之极 (豆瓣)1
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本书作者王骥是迄今为止中国唯一的艺术家手作书藏家，十几年来，他斥巨资收藏了200多本艺术家手作书，却始终蜗居在30㎡的小房子里。
2020年末，《书之极》一出版，旋即获选2020年“中国最美的书”。
书中呈现了24位艺术家的作品：有常玉、赵无极、萨尔瓦多·达利、安迪·沃霍尔、亨利·马蒂斯……甚至还有诺贝尔文学奖获得者君特·格拉斯。它展现了“书”这个载体做到极致能做成什么样子。
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- Feb 2021
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blogs.iteso.mx blogs.iteso.mx
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Preferimos pensar que quizás hay pocas mujeres que se embarcan en la carrera de concursos y proyectos de edificación de forma solitaria porque:
argumentación
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1.
puntos que son un llamado a la acción, vinculado al propósito
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Éstas y otras cuestiones se pusieron sobre la mesa la pasada semana en el 1º Congreso de Investigación en Arquitectura y Género “ArquitectAs: redefiniendo la profesión”, celebrado en la Escuela Técnica superior de Arquitectura de Sevilla y dirigido por Nuria Álvarez Lombardero, quien publicó el pasado mes en la ciudad viva un post de “presentación” al congreso. (Visitar aqui: http://www.laciudadviva.org/blogs/?p=20761)
citas, fuentes de consulta
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arstechnica.com arstechnica.com
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苹果准备最早明年发布它的高端 VR 设备，这款计划中的产品售价将会高达 3000 美元。代号为 N301 的 VR 设备使用了两个 8K 显示屏，采用 M1 芯片的继任者，能展示丰富的 3D 图形。苹果将会使用眼球跟踪技术以较低的保真度渲染非用户注视的目标。苹果正在测试的一个版本使用了 10 多个摄像头，从跟踪手运动到提供周围空间的即时动态，可用于混合和增强现实体验，不限于浸入式的 VR。
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logisticsofreligionblog.wordpress.com logisticsofreligionblog.wordpress.com
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For Latour, the ideology of neoliberalism has caused the operation of global capital to be elevated to the same order as that of inert matter: both are taken as fixed and obligatory realities that are entirely independent of the contingent behaviour of human beings in the world down-below.
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- Jan 2021
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watchit-desktop
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dimartinobooth.com dimartinobooth.com
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In the meantime, I invite you to partake of this week’s tribute to the current generation of traders who’ve withstood the destruction of price discovery at the hands of overly-intrusive central banking policy. Please enjoy, The Unbearable Lightness of Trading.
destruction of price discovery
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fckestructural.wordpress.com fckestructural.wordpress.com
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paraboloides hiperbólicos
Trabajo Superficie Activa
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chrisaldrich.wordpress.com chrisaldrich.wordpress.com
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Tag: marginalia
- for : TrailHub4Hypothesis
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