29 Matching Annotations
  1. Oct 2026
    1. Landscape of pathogenic variants in six pre-mRNA processing factor genes for retinitis pigmentosa based on large in-house data sets and database comparisons

      PMID: 35138024

      Gene: PRPF4

      HGNC: 17349

      Disease: retinitis pigmentosa 70

      MONDO: 0014400

      InheritancePattern: autosomal dominant

      Prevalence: The overall prevalence of retinitis pigmentosa is between 1 in 3,000 and 1 in 4,000 individuals, while the proportion of retinitis pigmentosa with a dominant mode of inheritance is estimated to be 15-35% (between 1 in 8,500 and 1 in 27,000). The proportion of that incidence made up by the specific form caused by variants in PRPF4 is not clear.

      Penetrance: Known disease-causing alleles appear to be incompletely penetrant (PMID: 25383878).

    1. Mutational screening of splicing factor genes in cases with autosomal dominant retinitis pigmentosa

      PMID: 24959063

      Gene: PRPF4

      HGNC: 17349

      Disease: retinitis pigmentosa 70

      MONDO: 0014400

      InheritancePattern: autosomal dominant

      Prevalence: The overall prevalence of retinitis pigmentosa is between 1 in 3,000 and 1 in 4,000 individuals, while the proportion of retinitis pigmentosa with a dominant mode of inheritance is estimated to be 15-35% (between 1 in 8,500 and 1 in 27,000). The proportion of that incidence made up by the specific form caused by variants in PRPF4 is not clear.

      Penetrance: Known disease-causing alleles appear to be incompletely penetrant (PMID: 25383878).

    2. We detected novel missense changes in individual patients in the sequence of the genes PRPF4 and EFTUD2, but the role of these changes in relationship to disease could not be verified.

      Case#: Benaglio_2014_Proband_001-417, sex not reported, age not reported, national origin German

      CasePresentingHPOs: N/A

      CaseHPOFreeText: The proband has been diagnosed with autosomal dominant retinitis pigmentosa.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Previous testing in the proband consisted of screening either by Sanger sequencing of 90% of known adRP genes, by genotyping microarray of known RP variants, or sequencing-based genotyping of RHO, RDS, PRPF31, RP1, PRPF8, IMPDH1, NRL, PRPF3, NR2E3, and SNRNP200.

      CaseMethod1: next-generation sequencing of PRPF4 and EFTUD2 genes

      CaseMethod2: Sanger sequencing of the coding regions of NHP2L1 and AAR2

      CaseGenotypingMethod: Genotyping of the proband initially consisted of either Sanger sequencing of 90% of known adRP genes, genotyping microarray of known RP variants, or sequencing-based genotyping of RHO, RDS, PRPF31, RP1, PRPF8, IMPDH1, NRL, PRPF3, NR2E3, and SNRNP200. Subsequent genotyping was performed by next-generation sequencing of PRPF4 and EFTUD2 genes and Sanger sequencing of the coding regions of NHP2L1 and AAR2.

      Variant: The proband harbors the NM_001244926.2(PRPF4):c.556C>G (p.Pro186Ala) variant in the heterozygous state.

      ClinVar ID: 865751

      gnomAD: The NM_001244926.2(PRPF4):c.556C>G (p.Pro186Ala) variant is found in gnomAD v4.1.0 at a frequency of 0.00006609 (90 alleles / 1180038 total alleles, with 0 homozygotes) in the European (non-Finnish) population https://gnomad.broadinstitute.org/variant/9-113283207-C-G?dataset=gnomad_r4

      VariantEvidence: NM_001244926.2(PRPF4):c.556C>G (p.Pro186Ala) is a missense variant located 5 bp from the 3' end of exon 5 with no direct evidence of an abnormal impact on the PRPF4 protein.

      CaseAddInfo: The proband has an affected sibling who also harbors the variant.

      CasePMIDs: N/A

    1. c.-114_-97del in a simplex RP patient

      Case#: Chen_2014_Proband_S01, male, age 20 years at onset, age 53 years at time of report, family origin reported as Chinese

      CasePresentingHPOs: Nyctalopia HP:0000662, Constriction of peripheral visual field HP:0001133, Severely reduced visual acuity HP:0001141, Undetectable electroretinogram HP:0000550, Retinal degeneration HP:0000546, Macular degeneration HP:0000608, Optic disc pallor HP:0000543, Attenuation of retinal blood vessels HP:0007843, Pigmentary retinopathy HP:0000580

      CaseHPOFreeText: The proband has been diagnosed with retinitis pigmentosa. Patient fibroblasts showed 92.58% decreased expression of PRPF4.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Previous testing in the proband included next-generation sequencing targeted to a large number of known variants in all known retinal disease-related genes.

      CaseMethod1: next-generation sequencing

      CaseMethod2: Sanger sequencing of PRPF4

      CaseGenotypingMethod: Genotyping of the proband included next-generation sequencing targeted to a large number of known variants in all known retinal disease-related genes, followed by Sanger sequencing analysis of all coding regions of PRPF4.

      Variant: The proband harbors the NM_004697.4(PRPF4):c.-114_-97del variant in the heterozygous state.

      ClinVar ID: 143058

      gnomAD: The NM_004697.4(PRPF4):c.-114_-97del variant is found in gnomAD v4.1.0 at a frequency of 0.0003297 (13 alleles / 39430 total alleles, with 0 homozygotes) in the East Asian population https://gnomad.broadinstitute.org/variant/9-113275629-TTGTCAGTGACGCACTTCC-T?dataset=gnomad_r4

      VariantEvidence: NM_004697.4(PRPF4):c.-114_-97del is a deletion variant within the 5' UTR that disrupts the beginning of the transcribed region. Luciferase assay indicates that the ability of the PRPF4 promoter to activate transcription of the reporter gene was significantly decreased by the variant, which disrupted binding sites for the c-Ets-1 and GR-alpha transcription factors and matched the 93% decrease in PRPF4 expression seen in the patient blood cells (Figure 3).

      CaseAddInfo: The proband has an unaffected son who does not harbor the variant.

      CasePMIDs: N/A

    2. Further, over expression of hPrp4(Pro315Leu), but not hPrp4(WT), triggered systemic deformities in wild-type zebrafish embryos with the retina primarily affected, and dramatically augmented death rates in morphant embryos, in which orthologous zebrafish prpf4 gene was silenced. We conclude that mutations of PRPF4 cause RP via haploinsufficiency and dominant-negative effects, and establish PRPF4 as a new U4/U6-U5 snRNP component associated with adRP.

      ExperimentName: "Variant overexpression in zebrafish causes defects in visual function."

      NonHumanModel: Danio rerio

      GeneAlteration: The model animals have been subjected to microinjection of PRPF4 mRNA (either wild-type or harboring the p.Pro315Leu variant), with expression levels comparable to the endogenous gene.

      ModelPhenotype: Photoreceptor layer loss on macular OCT HP:0030609, Inner retinal layer loss on macular OCT HP:0030620, Photoreceptor outer segment loss on macular OCT HP:0030610

      HumanPhenotype: Constriction of peripheral visual field HP:0001133, Reduced visual acuity HP:0007663,, Decreased light- and dark-adapted electroretinogram amplitude HP:0000654. Retinal degeneration HP:0000546, Macular degeneration HP:0000608, Optic disc pallor HP:0000543, Attenuation of retinal blood vessels HP:0007843, Pigmentary retinopathy HP:0000580

      ModelEvidence: The variant causes severely disrupted photoreceptors in the retina (Figure 5D), reduced rhodopsin staining (rod marker) in the IS/OS layer (Figures 5E-5J) and other deformities such as malformed brains, short trunks, cardiac edema and curved body axis, at higher levels than in the wild-type control (Figures 5B and 5C). The retinal transcripts opn1lw1, gnat2, rs1, snrpg, prph2b, gnb3, and rho were decreased in the variant-expressing zebrafish (Figure 5K), while the splicing factor transcripts prpf4, prpf3, prpf31, prpf6, prpf8, snrnp200, eftud2, and sart1 were increased (Figures 5A, 5L).

      ModelVariant: This model introduced the disease-associated variant NM_001244926.2(PRPF4):c.941C>T (p.Pro314Leu) in the heterozygous state (ClinVar ID: 143057).

    3. Here, we identified two heterozygous variants in PRPF4, including c.-114_-97del in a simplex RP patient and c.C944T (p.Pro315Leu), which co-segregates with disease phenotype in a family with adRP. Both variants were absent in 400 unrelated controls. The c.-114_-97del, predicted to affect two transcription factor binding sites, was shown to down-regulate the promoter activity of PRPF4 by a luciferase assay, and was associated with a significant reduction of PRPF4 expression in the blood cells of the patient. In fibroblasts from an affected individual with the p.Pro315Leu variant, the expression levels of several tri-snRNP components, including PRPF4 itself, were up-regulated, with altered expression pattern of SC35, a spliceosome marker. The same alterations were also observed in cells over expressing hPrp4(Pro315Leu), suggesting that they arose as a compensatory response to a compromised splicing mechanism caused by hPrp4 dysfunction.

      Case#: Chen_2014_Proband_AD01-II:3, male, age 15 years at time of first exam for poor night vision, age 58 years at time of report, family origin reported as Han Chinese

      CasePresentingHPOs: Nyctalopia HP:0000662, Constriction of peripheral visual field HP:0001133, Reduced visual acuity HP:0007663, Cataract HP:0000518, Retinal degeneration HP:0000546, Macular degeneration HP:0000608, Optic disc pallor HP:0000543, Attenuation of retinal blood vessels HP:0007843, Pigmentary retinopathy HP:0000580, Central thinning of the outer nuclear layer of the retina HP:6000367, Decreased light- and dark-adapted electroretinogram amplitude HP:0000654

      CaseHPOFreeText: The proband has been diagnosed with autosomal dominant retinitis pigmentosa, with features including complete loss of outer/inner segments (OS/IS) by OCT. Patient fibroblasts showed increased expression of PRPF3, PRPF6, PRPF8, PRPF31, EFTUD2, SART1, and PRPF4 itself.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Previous testing in the proband included next-generation sequencing targeted to a large number of known variants in all known retinal disease-related genes.

      CaseMethod1: next-generation sequencing

      CaseMethod2: Sanger sequencing of PRPF4

      CaseGenotypingMethod: Genotyping of the proband included next-generation sequencing targeted to a large number of known variants in all known retinal disease-related genes, followed by Sanger sequencing analysis of all coding regions of PRPF4.

      Variant: The proband harbors the NM_001244926.2(PRPF4):c.941C>T (p.Pro314Leu) variant in the heterozygous state.

      ClinVar ID: 143057

      gnomAD: The NM_001244926.2(PRPF4):c.941C>T (p.Pro314Leu) variant is found in gnomAD v4.1.0 at a frequency of 0.000003390 (4 alleles / 1179980 total alleles, with 0 homozygotes) in the European (non-Finnish) population https://gnomad.broadinstitute.org/variant/9-113288183-C-T?dataset=gnomad_r4

      VariantEvidence: NM_001244926.2(PRPF4):c.941C>T (p.Pro314Leu) is a missense variant. When over-expressed in zebrafish, the variant causes severely disrupted photoreceptors in the retina and other deformities such as malformed brains, short trunks, cardiac edema and curved body axis, unlike the wild-type control.

      CaseAddInfo: The proband has two similarly affected siblings (with onset in their 20's) and an unaffected child (approximately age 10 years) who also harbor the variant.

      CasePMIDs: N/A

    4. PRPF4 mutations cause autosomal dominant retinitis pigmentosa

      PMID: 24419317

      Gene: PRPF4

      HGNC: 17349

      Disease: retinitis pigmentosa 70

      MONDO: 0014400

      InheritancePattern: autosomal dominant

      Prevalence: The overall prevalence of retinitis pigmentosa is between 1 in 3,000 and 1 in 4,000 individuals, while the proportion of retinitis pigmentosa with a dominant mode of inheritance is estimated to be 15-35% (between 1 in 8,500 and 1 in 27,000). The proportion of that incidence made up by the specific form caused by variants in PRPF4 is not clear.

      Penetrance: Known disease-causing alleles appear to be incompletely penetrant (PMID: 25383878).

    5. The non-snRNP factors are also necessary for splicing, of which serine/arginine (SR)-rich proteins were considered as markers of splicing speckles (25). We determined whether p.Pro315Leu could affect the pattern of splicing speckles using SC-35, a non-snRNP component, as a marker (25). We performed immunofluorescence and Q-PCR on cells carrying either p.Pro315Leu or WT allele. By confocal microscopy, we found the level of endogenous SC-35 is dramatically increased with a diffused pattern in hPrp4Pro315Leu fibroblasts, whereas in control fibroblasts the SC-35 showed a distinctly speckled pattern (Fig. 4B and C). Consistently, Q-PCR revealed that the expression levels of SRSF1 (encoding SF2/ASF; NM_006924.4), another non-snRNP component and SRSF2 (encoding SC-35; NM_003016.4) were significantly increased in hPrp4Pro315Leu fibroblasts compared with WT fibroblasts (Fig. 4A). Similar changes in the levels and distribution of SC-35 were also observed in ARPE19 and 293T cells transfected with hPrp4Pro315Leu, but not in those transfected with hPrp4WT (Fig. 4D–G), indicating that the p.Pro315Leu variant of PRPF4 affected the splicing machinery.

      ExperimentName: Altered pattern of splicing speckles in patient fibroblasts harboring a heterozygous p.Pro315Leu variant in PRPF4

      PatientCell: CL:0000057 (fibroblast)

      GeneFunction: GO:0000398 (mRNA splicing, via spliceosome)

      GeneAlteration: Cells harbor a heterozygous p.Pro315Leu variant in PRPF4.

      FunctionalEvidence: Patient cells harboring the variant exhibit a much higher level of endogenous marker of splicing speckles (SC-35) with a diffused distribution rather than a pattern of distinct speckles (Figures 4B and 4C). RT-PCR showed increased expression of SRSF1 and SRSF2 as well (Figure 4A). Collectively, the patient cells harboring the variant show molecular evidence of disrupted splicing.

      FAVariants: The model harbors the NM_001244926.2(PRPF4):c.941C>T (p.Pro314Leu) variant in the heterozygous state (ClinVar ID: 143057).

    1. Hprp3p and Hprp4p have been shown to interact with each other and the first 100 amino acids of Hprp3p are not essential for this interaction. These experiments suggest that both Hprp3p and Hprp4p are components of human spliceosomes.

      ExperimentName: PRPF4 physically interacts with PRPF3.

      InteractingGene: PRPF3 (HGNC:17348)

      InteractionType: Physical

      InteractionMethod: Co-immunoprecipitation

      InteractionEvidence: Immunoprecipitation of endogenous PRPF3 from HeLa cell nuclear extracts pulled down PRPF4 (Figures 5 and 6).

    2. Identification and characterization of human genes encoding Hprp3p and Hprp4p, interacting components of the spliceosome

      PMID: 9328476

      Gene: PRPF4

      HGNC: 17349

      Disease: retinitis pigmentosa 70

      MONDO: 0014400

      InheritancePattern: autosomal dominant

      Prevalence: The overall prevalence of retinitis pigmentosa is between 1 in 3,000 and 1 in 4,000 individuals, while the proportion of retinitis pigmentosa with a dominant mode of inheritance is estimated to be 15-35% (between 1 in 8,500 and 1 in 27,000). The proportion of that incidence made up by the specific form caused by variants in PRPF4 is not clear.

      Penetrance: Known disease-causing alleles appear to be incompletely penetrant (PMID: 25383878).

    1. Silencing of Prpf4, a splicing factor hitherto unrelated to RP, evoked the same defects in vision, photoreceptor morphology and retinal gene expression. Hence, various routes affecting the tri-snRNP can elicit tissue-specific gene expression defects and lead to the RP phenotype.

      ExperimentName: "Prpf4 silencing in zebrafish causes defects in visual function."

      NonHumanModel: Danio rerio

      GeneAlteration: The model animals have been subjected to morpholino-based knockdown of Prpf4, the zebrafish ortholog of human PRPF4.

      ModelPhenotype: Nystagmus HP:0000639, Abnormality of ocular smooth pursuit HP:0000617

      HumanPhenotype: Constriction of peripheral visual field HP:0001133, Reduced visual acuity HP:0007663,, Decreased light- and dark-adapted electroretinogram amplitude HP:0000654. Retinal degeneration HP:0000546, Macular degeneration HP:0000608, Optic disc pallor HP:0000543, Attenuation of retinal blood vessels HP:0007843, Pigmentary retinopathy HP:0000580

      ModelEvidence: Morpholino-based incomplete knockdown of the Prpf4 gene circumvents the lethality of complete silencing and causes optokinetic nystagmus with a significantly reduced number of saccades (Fig. 5B, 5C, 5D). Immunohistochemistry showed that retinal morphology showed mostly normal retinal layering but decreased rhodopsin staining in the photoreceptor cell layer (Figs. 5E–5H). Photoreceptor outer segments were primarily affected, but with unaffected cell body morphology (Figs. 5I and 5J). This phenotype was a complete match for the zebrafish with Prpf31 loss/. Semi-quantitative RT–PCR analysis of the RP-relevant transcripts opn1lw1, opn1mw1, gnat2, irx6a, rx3, crx and rhodopsin as well as the controls gapdh and lsm7 showed a very similar pattern of down-regulation in both Prpf31- and Prpf4-deficient animals (Fig. 5W). The phenotype was dose-dependent and could be rescued by co-injection of Prpf4 mRNA (Fig. S2).

      ModelVariant: This model did not introduce a disease-associated variant known from an affected human patient, but rather studied the effects of heterozygous loss of the gene product.

    2. Systemic splicing factor deficiency causes tissue-specific defects: a zebrafish model for retinitis pigmentosa

      PMID: 21051334

      Gene: PRPF4

      HGNC: 17349

      Disease: retinitis pigmentosa 70

      MONDO: 0014400

      InheritancePattern: autosomal dominant

      Prevalence: The overall prevalence of retinitis pigmentosa is between 1 in 3,000 and 1 in 4,000 individuals, while the proportion of retinitis pigmentosa with a dominant mode of inheritance is estimated to be 15-35% (between 1 in 8,500 and 1 in 27,000). The proportion of that incidence made up by the specific form caused by variants in PRPF4 is not clear.

      Penetrance: Known disease-causing alleles appear to be incompletely penetrant (PMID: 25383878).

    1. Combining a prioritization strategy and functional studies nominates 5'UTR variants underlying inherited retinal disease

      PMID: 38184646

      Gene: PRPF4

      HGNC: 17349

      Disease: retinitis pigmentosa 70

      MONDO: 0014400

      InheritancePattern: autosomal dominant

      Prevalence: The overall prevalence of retinitis pigmentosa is between 1 in 3,000 and 1 in 4,000 individuals, while the proportion of retinitis pigmentosa with a dominant mode of inheritance is estimated to be 15-35% (between 1 in 8,500 and 1 in 27,000). The proportion of that incidence made up by the specific form caused by variants in PRPF4 is not clear.

      Penetrance: Known disease-causing alleles appear to be incompletely penetrant (PMID: 25383878).

    2. PRPF4

      Case#: Dueñas Rey_2024_Proband_F11, sex and age not reported, part of cohort from Center for Medical Genetics Ghent

      CasePresentingHPOs: Rod-cone dystrophy HP:0000510, Intellectual disability HP:0001249

      CaseHPOFreeText: The proband has been diagnosed with rod-cone dystrophy and clinical signs of Bardet-Biedl syndrome. Intellectual disability may be part of the phenotype.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Previous testing in the proband consisted of whole exome sequencing with analysis focused on the 5' UTR regions of 378 genes highly expressed in the retina.

      CaseMethod1: whole exome sequencing

      CaseMethod2: Sanger sequencing of the coding regions of PRPF4

      CaseGenotypingMethod: Genotyping of the proband initially consisted of whole exome sequencing, followed by Sanger sequencing of the coding regions of PRPF4.

      Variant: The proband harbors the NM_001244926.2:c.-6C>T variant in the heterozygous state.

      CAID: CA2579423618

      gnomAD: The NM_001244926.2:c.-6C>T variant is found in gnomAD v4.1.0 at a frequency of 8.400e-7 (4 alleles / 1178930 total alleles, with 0 homozygotes) in the European (non-Finnish) population https://gnomad.broadinstitute.org/variant/9-113275738-C-T?dataset=gnomad_r4

      VariantEvidence: NM_001244926.2:c.-6C>T is a 5' UTR variant located within the Kozak consensus sequence but has no direct evidence of an abnormal impact on PRPF4 expression.

      CaseAddInfo: The proband has apparently unaffected parents.

      CasePMIDs: N/A

    1. We demonstrate that the 60 and 90kD tri-snRNP proteins specifically associate with the U4/U6 snRNP at salt concentrations where the tri-snRNP complex has dissociated. The primary structures of the 60kD and 90kD proteins were determined by cloning and sequencing their respective cDNAs. The U4/U6-60kD protein possesses a C-terminal WD domain that contains seven WD repeats and thus belongs to the WD-protein family, whose best-characterized members include the Gbeta subunits of heterotrimeric G proteins. A database homology search revealed a significant degree of overall homology (57.8% similarity, 33.9% identity) between the human 60kD protein and the Saccharomyces cerevisiae U4/U6 snRNP protein Prp4p. Two additional, previously undetected WD repeats (with seven in total) were also identified in Prp4p, consistent with the possibility that 60kD/Prp4p, like beta-transducin, may adopt a propeller-like structure. The U4/U6-90kD protein was shown to exhibit significant homology, particularly in its C-terminal half, with the S. cerevisiae splicing factor Prp3p, which also associates with the yeast U4/U6 snRNP. Interestingly, U4/U6-90kD shares short regions of homology with E. coli RNase III, including a region encompassing its double-stranded RNA binding domain. Based on their structural similarity with essential splicing factors in yeast, the human U4/U6-60kD and 90kD proteins are likely also to play important roles in the mammalian splicing process.

      Selection A- Gene with same function implicated in disease

      ExperimentName: PRPF4 is a U4/U6 small nuclear ribonucleoprotein component that functions in mRNA splicing.

      GOterm: GO:0000398 (mRNA splicing, via spliceosome)

      FunctionalEvidence: PRPF4, PRPF3, PRPF31, and PRPF8 are all splicing factors involved in mRNA processing and are encoded by genes that harbor variants associated with retinitis pigmentosa.

      HGNC: HGNC:17348 (PRPF3, retinitis pigmentosa 18), HGNC:15446 (PRPF31, retinitis pigmentosa 11), HGNC:17340 (PRPF8, retinitis pigmentosa 13)

      GeneEvidence: PRPF3 harbors variants that cause retinitis pigmentosa 18 (PMID: 11773002), PRPF31 harbors variants that cause retinitis pigmentosa 11 (PMID: 12444105), and PRPF8 harbors variants that cause retinitis pigmentosa 13 (PMID: 7951236).

      SharedGeneImplication: PRPF4, PRPF3, PRPF31, and PRPF8 are encode splicing factors involved in mRNA processing.

    2. The human U4/U6 snRNP contains 60 and 90kD proteins that are structurally homologous to the yeast splicing factors Prp4p and Prp3p

      PMID: 9257651

      Gene: PRPF4

      HGNC: 17349

      Disease: retinitis pigmentosa 70

      MONDO: 0014400

      InheritancePattern: autosomal dominant

      Prevalence: The overall prevalence of retinitis pigmentosa is between 1 in 3,000 and 1 in 4,000 individuals, while the proportion of retinitis pigmentosa with a dominant mode of inheritance is estimated to be 15-35% (between 1 in 8,500 and 1 in 27,000). The proportion of that incidence made up by the specific form caused by variants in PRPF4 is not clear.

      Penetrance: Known disease-causing alleles appear to be incompletely penetrant (PMID: 25383878).

    1. Our results revealed that the PRPF31 deficiency causes mis-splicing of genes involved in RNA processing (PRPF3, PRPF8, PRPF4, and PRPF19) and phototransduction (RHO, ROM1, FSCN2, GNAT2, and GNAT1) in the retina in the PRPF31 reduced samples. Mis-splicing of genes implicated in phototransduction was associated with photoreceptor degeneration observed in RP patients.

      PRPF4, PRPF3, PRPF31, and PRPF8 are all splicing factors involved in mRNA processing and are encoded by genes that harbor variants associated with retinitis pigmentosa.

    1. Here, we report the identification of the p.R192H variant of the tri-snRNP factor PRPF4 in a patient with RP. The mutation affects a highly conserved arginine residue that is crucial for PRPF4 function. Introduction of a corresponding mutation into the zebrafish homolog of PRPF4 resulted in a complete loss of function in vivo. A series of biochemical experiments suggested that p.R192H disrupts the binding interface between PRPF4 and its interactor PRPF3. This interferes with the ability of PRPF4 to integrate into the tri-snRNP, as shown in a human cell line and in zebrafish embryos. These data suggest that the p.R192H variant of PRPF4 represents a functional null allele. The resulting haploinsufficiency of PRPF4 compromises the function of the tri-snRNP, reinforcing the notion that this spliceosomal particle is of crucial importance in the physiology of the retina.

      Case#: Linder_2014_Proband_RP-106, female, age 20 years at time of onset / first visual complaints, age 73 year at time of report, family origin not reported

      CasePresentingHPOs: Nyctalopia HP:0000662, Constriction of peripheral visual field HP:0001133, Cataract HP:0000518, Attenuation of retinal blood vessels HP:0007843, Bone spicule pigmentation of the retina HP:0007737, Undetectable dark-adapted electroretinogram HP:0030474, Decreased light- and dark-adapted electroretinogram amplitude HP:0000654

      CaseHPOFreeText: The proband has been diagnosed with sporadic retinitis pigmentosa. Phenotypes included pale papillae in fundus.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Previous testing in the proband was not clearly described, but she was part of a cohort of patients with no previously-identified retinitis pigmentosa-associated variants.

      CaseMethod1: SSCP analysis of 14 PCR-amplified PRPF4 exons

      CaseMethod2: Sanger sequencing of PRPF4

      CaseGenotypingMethod: Previous testing in the proband was not clearly described, but she was part of a cohort of patients with no previously-identified retinitis pigmentosa-associated variants. SSCP was performed on each of 14 PCR-amplified exons of PRPF4, followed by Sanger sequencing analysis.

      Variant: The proband harbors the NM_001244926.2(PRPF4):c.572G>A (p.Arg191His) variant in the heterozygous state.

      ClinVar ID: 967144

      gnomAD: The NM_001244926.2(PRPF4):c.572G>A (p.Arg191His) variant is found in gnomAD v4.1.0 at a frequency of 0.00004999 (3 / 60014, with 0 homozygotes) in the Admixed American population https://gnomad.broadinstitute.org/variant/9-113283400-G-A?dataset=gnomad_r4

      VariantEvidence: NM_001244926.2(PRPF4):c.572G>A (p.Arg191His) is a missense variant. When overexpressed in zebrafish, the variant fails to rescue the lethality of Prpf4 silencing, unlike overexpression of the wild-type gene (Figure 2). Co-immunoprecipitation experiments show that the variant localizes normally but disrupts interaction with PRPF3 (Figure 3) and blocks PRPF4 integration into snRNP complexes (Figure 4).

      CaseAddInfo: The proband has two daughters at ages 52 and 54 years who harbor the variant but showed no retinal abnormalities in ophthalmological examinations.

      CasePMIDs: N/A

    2. Identification of a PRPF4 loss-of-function variant that abrogates U4/U6.U5 tri-snRNP integration and is associated with retinitis pigmentosa

      PMID: 25383878

      Gene: PRPF4

      HGNC: 17349

      Disease: retinitis pigmentosa 70

      MONDO: 0014400

      InheritancePattern: autosomal dominant

      Prevalence: The overall prevalence of retinitis pigmentosa is between 1 in 3,000 and 1 in 4,000 individuals, while the proportion of retinitis pigmentosa with a dominant mode of inheritance is estimated to be 15-35% (between 1 in 8,500 and 1 in 27,000). The proportion of that incidence made up by the specific form caused by variants in PRPF4 is not clear.

      Penetrance: Known disease-causing alleles appear to be incompletely penetrant (PMID: 25383878).

    1. The network of protein–protein interactions within the human U4/U6.U5 tri-snRNP

      PMID: 16723661

      Gene: PRPF4

      HGNC: 17349

      Disease: retinitis pigmentosa 70

      MONDO: 0014400

      InheritancePattern: autosomal dominant

      Prevalence: The overall prevalence of retinitis pigmentosa is between 1 in 3,000 and 1 in 4,000 individuals, while the proportion of retinitis pigmentosa with a dominant mode of inheritance is estimated to be 15-35% (between 1 in 8,500 and 1 in 27,000). The proportion of that incidence made up by the specific form caused by variants in PRPF4 is not clear.

      Penetrance: Known disease-causing alleles appear to be incompletely penetrant (PMID: 25383878).

    1. Prpf4 (pre-mRNA processing factor 4), a key component of spliceosome, plays critical roles in pre-mRNA splicing and its mutations result in retinitis pigmentosa due to photoreceptor defects. In this study, we characterized a zebrafish prpf4t243 mutant harboring a Tol2 transposon-based gene trap cassette in the third intron of the prpf4 gene. Cells in the brain and spinal cord gradually undergo p53-dependent apoptosis after 28 hpf in prpf4t243 mutants, suggesting that a widespread function of prpf4 in neural cell survival. In addition, prpf4 is essential for survival of posterior lateral line primordial (pLLP) cells. prpf4 deficiency perturbs Fgf, Wnt/β-catenin and chemokine signaling pathways and impairs pLLP migration. RNA-Seq analysis suggests that prpf4 deficiency may impair spliceosome assembly, leading to compensatory upregulation of core spliceosomal genes and alteration of pre-mRNA splicing. Taken together, our studies uncover an essential role of prpf4 in pre-mRNA splicing, cell survival and pLLP migration.

      Zebrafish harboring an engineered mutation in the prpf4 gene exhibit enhanced brain and spinal cord apoptosis. The mechanism is loss-of-function. Matches the patients?

    1. Clinical and whole exome sequencing findings in children from Yunnan Yi minority ethnic group with retinitis pigmentosa: two case reports

      PMID: 37264419

      Gene: PRPF4

      HGNC: 17349

      Disease: retinitis pigmentosa 70

      MONDO: 0014400

      InheritancePattern: autosomal dominant

      Prevalence: The overall prevalence of retinitis pigmentosa is between 1 in 3,000 and 1 in 4,000 individuals, while the proportion of retinitis pigmentosa with a dominant mode of inheritance is estimated to be 15-35% (between 1 in 8,500 and 1 in 27,000). The proportion of that incidence made up by the specific form caused by variants in PRPF4 is not clear.

      Penetrance: Known disease-causing alleles appear to be incompletely penetrant (PMID: 25383878).

    2. Here, we used whole-exome sequencing to detect mutations in the genes of the probands of the retinitis pigmentosa families, and Sanger sequencing to confirm the causal mutations identified by whole exome sequencing. In addition, we report two cases with retinitis pigmentosa caused by RDH12 (c.524C > T) and PRPF4 (c.1273G > A) pathogenic mutations.

      Case#: Xiao_2023_Family_2_Proband, male, age 0.5 years, family origin reported as from Yi ethnic group from Yunnan, China

      CasePresentingHPOs: Infantile onset HP:0003593, Pigmentary retinopathy HP:0000580, Mild myopia HP:0025573

      CaseHPOFreeText: The proband has been diagnosed with retinitis pigmentosa with onset at 0.3 years of age.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Previous testing in the proband consisted of whole exome sequencing.

      CaseMethod1: whole exome sequencing

      CaseMethod2: Sanger sequencing of the coding regions of PRPF4

      CaseGenotypingMethod: Genotyping of the proband initially consisted of whole exome sequencing, followed by Sanger sequencing of the coding regions of PRPF4.

      Variant: The proband harbors the NM_001244926.2(PRPF4):c.1270G>A (p.Gly424Ser) variant in the heterozygous state.

      ClinVar ID: 1395419

      gnomAD: The NM_001244926.2(PRPF4):c.1270G>A (p.Gly424Ser) variant is found in gnomAD v4.1.0 at a frequency of 0.00008729 (103 alleles / 1180028 total alleles, with 0 homozygotes) in the European (non-Finnish) population https://gnomad.broadinstitute.org/variant/9-113290914-G-A?dataset=gnomad_r4

      VariantEvidence: NM_001244926.2(PRPF4):c.1270G>A (p.Gly424Ser) is a missense variant with no direct evidence of an abnormal impact on the PRPF4 protein.

      CaseAddInfo: The proband has apparently unaffected parents.

      CasePMIDs: N/A

    1. Within the PRPF4 sequence, we identified two annotated variants, p.His78Arg and p.Pro187Ala (Table 2). The first one corresponded to dbSNP entry rs1138958 and was present in 60 European heterozygotes from the Exome Variant Server database; therefore, we considered the variant to be non-pathogenic. The second variant, found in a single individual (ID: 001–417), involved nucleotide c.559C (NM_004697.3, exon 5), which was flagged in dbSNP as entry rs187531407 and referred to a CCC>TCC (p.Pro187Ser) change, found only in two non-validated 1000 Genomes reports. We ascertained that one of these reports (a low-coverage genome in an African sample) was a false positive, following validation with direct Sanger sequencing on the original DNA sample (ID: NA18933, Coriell DNA repository). Moreover, although the nucleotide is the same, the base change in the patient in our cohort was different compared to rs187531407. More specifically, we identified a CCC>GCC change, which resulted in p.Pro187Ala. Proline 187 is not fully conserved across different species and, according to predictions with different tools, the likelihood of pathogenicity of p.Pro187Ala is uncertain (Table 3). We followed up this change by analyzing controls and available relatives. Public databases, as well as sequencing of in-house controls, did not reveal the presence of this change. We then screened an additional 202 patients with adRP from the same cohorts for this specific variant, but this change was not found in any additional individuals. The affected sibling (ID: 226–1953) of the index patient also carried the same change, but other family members were not available for further segregation analysis. Since the base change is located within exon 5, at a 5-bp distance from the donor splice site, we also checked if splicing of this exon was affected. Bioinformatic prediction was negative, and reverse-transcription (RT)–PCR of patient’s cDNA did not reveal missplicing events. In the absence of additional elements, we could neither exclude nor validate this change as a potential mutation.

      Case#: Benaglio_2014_Proband_001-417, sex not reported, age not reported, national origin German

      CasePresentingHPOs: N/A

      CaseHPOFreeText: The proband has been diagnosed with autosomal dominant retinitis pigmentosa.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Previous testing in the proband consisted of screening either by Sanger sequencing of 90% of known adRP genes, by genotyping microarray of known RP variants, or sequencing-based genotyping of RHO, RDS, PRPF31, RP1, PRPF8, IMPDH1, NRL, PRPF3, NR2E3, and SNRNP200.

      CaseMethod1: next-generation sequencing of PRPF4 and EFTUD2 genes

      CaseMethod2: Sanger sequencing of the coding regions of NHP2L1 and AAR2

      CaseGenotypingMethod: Genotyping of the proband initially consisted of either Sanger sequencing of 90% of known adRP genes, genotyping microarray of known RP variants, or sequencing-based genotyping of RHO, RDS, PRPF31, RP1, PRPF8, IMPDH1, NRL, PRPF3, NR2E3, and SNRNP200. Subsequent genotyping was performed by next-generation sequencing of PRPF4 and EFTUD2 genes and Sanger sequencing of the coding regions of NHP2L1 and AAR2.

      Variant: The proband harbors the NM_001244926.2(PRPF4):c.556C>G (p.Pro186Ala) variant in the heterozygous state.

      ClinVar ID: 865751

      gnomAD: The NM_001244926.2(PRPF4):c.556C>G (p.Pro186Ala) variant is found in gnomAD v4.1.0 at a frequency of 0.00006609 (90 alleles / 1180038 total alleles, with 0 homozygotes) in the European (non-Finnish) population https://gnomad.broadinstitute.org/variant/9-113283207-C-G?dataset=gnomad_r4

      VariantEvidence: NM_001244926.2(PRPF4):c.556C>G (p.Pro186Ala) is a missense variant located 5 bp from the 3' end of exon 5 with no direct evidence of an abnormal impact on the PRPF4 protein.

      CaseAddInfo: The proband has an affected sibling who also harbors the variant.

      CasePMIDs: N/A