Here we demonstrate that β-catenin activity is a key target of polarity specification in planarians,
This is a well-supported conclusion for this paper
Here we demonstrate that β-catenin activity is a key target of polarity specification in planarians,
This is a well-supported conclusion for this paper
In Smedβ-catenin-a(RNAi) and SmedDvl-a/b(RNAi) worms, the “posterior” head expressed the anterior marker and the posterior marker was severely reduced or absent
this likely means that the system nearly fully recognized that wound site as the anterior end instead of posterior now.
To address whether these changes were superficial or reflected a fate transformation of internal cell types and organ systems, we utilized anatomical and molecular markers of A/P identity.
Here they are about to include markers to test if this happened by chance or if their hypothesis is still supported. It seems to me that they also could have done a few repetitions of the study to confirm it was not by chance
APC is an essential member of a destruction complex that phosphorylates β-catenin,
interesting that APC is used to prevent head formation by degrading b-catenin, is it expressing everywhere except for the head? how exactly does it differentiate the cells
formed a brain in the tail region
I know they say that the new head move autonomously from the rest of the body, I wonder how much control this new brain has over the body and if it is fully/properly developed.
By day 14, in addition to a new head, moving head-like protrusions developed from the periphery (Fig. 4C,F; Movie S5). Similar protrusions also developed in trunk fragments (Movie
This is very odd, I wonder if these spots may have been accidentally wounded and so the body thinks it needs to grow a head there (if maybe wounds are also regulated by catenin and ACP) or if its something similar to how mutation in these genes in humans can cause cancerous growths
Although we cannot rule out protein perdurance, incomplete gene silencing, or redundancy
This may not be a great question but I wonder if this is transient or stable. If the worms that grew a head where its tail should be were amputated again would it grow back wrong again?
It is interesting that we did not observe any head or tail mis-specification phenotypes for any of the upstream components of canonical Wnt signaling
Ist it really that interesting? to me it seems that an upstream component would not affect the specification because it does not matter yet, the pathways start out the same and then diverge based on ACP/beta-catenin
In adult animals, the Wnt/β-catenin pathway participates in regeneration and tissue homeostasis, while pathway misregulation can lead to degenerative diseases and cancer in humans
It is fascinating that research on a gene in planarians regeneration of body parts can give us information as to how misregulation in these same genes leads to cancer and degenerative diseases in humans.
Signaling through β-catenin defines head vs. tail during regeneration.
figure 1 seems to support their hypothesis as the control group regenerated head and tail as expected, the b-catenin group did not regenerate a tail and a second head was regenerated instead, Dvl-a/b did not regenerate at all, and APC regenerated tails at both ends with no head.