ArticleNucleic acids research2021
Prpf31 is essential for the survival and differentiation of retinal progenitor cells by modulating alternative splicing.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Integrated multi-omics identifies macrophage ARG1-mediated deacetylation with causal and diagnostic implications in ischemic stroke.iScience · 2026Article
- Decoding retinitis pigmentosa: molecular targets and therapy with focus on pre-mRNA splicing.Cellular and molecular life sciences : CMLS · 2025Review
- Alternative Splicing Dysregulation in Retinitis Pigmentosa: Pathogenic Mechanisms and Therapeutic Opportunities.Biomolecules · 2025Review
- RPGRORF15 Mutations Disrupt Lysosomal Lipid Metabolism in Retinal Pigment Epithelium Cells and Cause Retinitis Pigmentosa.Investigative ophthalmology & visual science · 2025Article
- Intermittent fasting attenuates glial hyperactivation and photoreceptor degeneration in a NaIOCommunications biology · 2025Article
- Alternative splicing in stem cells and development: research progress and emerging technologies.Cell regeneration (London, England) · 2025Review
- Knockout ofBiomedicines · 2024Article
- Quantum Dots-caused Retinal Degeneration in Zebrafish Regulated by Ferroptosis and Mitophagy in Retinal Pigment Epithelial Cells through Inhibiting Spliceosome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Mutant kri1l causes abnormal retinal development via cell cycle arrest and apoptosis induction.Cell death discovery · 2024Article
- A Mettl16/mThe EMBO journal · 2024Article
- Therapeutic role of PTEN in tissue regeneration for management of neurological disorders: stem cell behaviors to an in-depth review.Cell death & disease · 2024Review
- RNA-binding proteins potentially regulate the alternative splicing of cell cycle-associated genes in proliferative diabetic retinopathy.Scientific reports · 2024Article
- The splicing factor Prpf31 is required for hematopoietic stem and progenitor cell expansion during zebrafish embryogenesis.The Journal of biological chemistry · 2024Article
- Deficiency of copper responsive gene stmn4 induces retinal developmental defects.Cell biology and toxicology · 2024Article
- PRPF31-retinitis pigmentosa: Challenges and opportunities for clinical translation.Vision research · 2023Review
- The splicing factor DHX38 enables retinal development through safeguarding genome integrity.iScience · 2023Article
- Alternative RNA Splicing in the Retina: Insights and Perspectives.Cold Spring Harbor perspectives in medicine · 2023Review
- Bifunctional MXene-Augmented Retinal Progenitor Cell Transplantation for Retinal Degeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Tulp1 deficiency causes early-onset retinal degeneration through affecting ciliogenesis and activating ferroptosis in zebrafish.Cell death & disease · 2022Article
- The emerging significance of splicing in vertebrate development.Development (Cambridge, England) · 2022Review
Corrections and comments
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Authors and funding
20 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysfunction of splicing factors often result in abnormal cell differentiation and apoptosis, especially in neural tissues. Mutations in pre-mRNAs processing factor 31 (PRPF31) cause autosomal dominant retinitis pigmentosa, a progressive retinal degeneration disease. The transcriptome-wide splicing events specifically regulated by PRPF31 and their biological roles in the development and maintenance of retina are still unclear. Here, we showed that the differentiation and viability of retinal progenitor cells (RPCs) are severely perturbed in prpf31 knockout zebrafish when compared with other tissues at an early embryonic stage. At the cellular level, significant mitotic arrest and DNA damage were observed. These defects could be rescued by the wild-type human PRPF31 rather than the disease-associated mutants. Further bioinformatic analysis and experimental verification uncovered that Prpf31 deletion predominantly causes the skipping of exons with a weak 5' splicing site. Moreover, genes necessary for DNA repair and mitotic progression are most enriched among the differentially spliced events, which may explain the cellular and tissular defects in prpf31 mutant retinas. This is the first time that Prpf31 is demonstrated to be essential for the survival and differentiation of RPCs during retinal neurogenesis by specifically modulating the alternative splicing of genes involved in DNA repair and mitosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.