ArticleGenetics2009
A genetic screen for suppressors of a mutated 5' splice site identifies factors associated with later steps of spliceosome assembly.
Article in Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- A role for SNU66 in maintaining 5' splice site identity during spliceosome assembly.RNA (New York, N.Y.) · 2024Article
- A forward genetic screen in C. elegans identifies conserved residues of spliceosomal proteins PRP8 and SNRNP200/BRR2 with a role in maintaining 5' splice site identity.Nucleic acids research · 2022Article
- A genetic screen in C. elegans reveals roles for KIN17 and PRCC in maintaining 5' splice site identity.PLoS genetics · 2022Article
- An SMU Splicing Factor Complex Within Nuclear Speckles Contributes to Magnesium Homeostasis in Arabidopsis.Plant physiology · 2020Article
- mRNA Editing, Processing and Quality Control inGenetics · 2020Review
- Destabilization of the human RED-SMU1 splicing complex as a basis for host-directed antiinfluenza strategy.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Prp8 impacts cryptic but not alternative splicing frequency.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- SNRP-27, theRNA (New York, N.Y.) · 2018Article
- Recruitment of RED-SMU1 complex by Influenza A Virus RNA polymerase to control Viral mRNA splicing.PLoS pathogens · 2014Article
- Article
- Given dimensions of neoplastic events as aberrantly operative alternative splicing.Pathology research international · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Many alleles of human disease genes have mutations within splicing consensus sequences that activate cryptic splice sites. In Caenorhabditis elegans, the unc-73(e936) allele has a G-to-U mutation at the first base of the intron downstream of exon 15, which results in an uncoordinated phenotype. This mutation triggers cryptic splicing at the -1 and +23 positions and retains some residual splicing at the mutated wild-type (wt) position. We previously demonstrated that a mutation in sup-39, a U1 snRNA gene, suppresses e936 by increasing splicing at the wt splice site. We report here the results of a suppressor screen in which we identify three proteins that function in cryptic splice site choice. Loss-of-function mutations in the nonessential splicing factor smu-2 suppress e936 uncoordination through changes in splicing. SMU-2 binds SMU-1, and smu-1(RNAi) also leads to suppression of e936. A dominant mutation in the conserved C-terminal domain of the C. elegans homolog of the human tri-snRNP 27K protein, which we have named SNRP-27, suppresses e936 uncoordination through changes in splicing. We propose that SMU-2, SMU-1, and SNRP-27 contribute to the fidelity of splice site choice after the initial identification of 5' splice sites by U1 snRNP.
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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 OpenQuestion graph.