ArticleGenetics2000
The allele-specific suppressor sup-39 alters use of cryptic splice sites in Caenorhabditis elegans.
Article in Genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 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
- mRNA Editing, Processing and Quality Control inGenetics · 2020Review
- HRP-2, the Caenorhabditis elegans homolog of mammalian heterogeneous nuclear ribonucleoproteins Q and R, is an alternative splicing factor that binds to UCUAUC splicing regulatory elements.The Journal of biological chemistry · 2009Article
- A genetic screen for suppressors of a mutated 5' splice site identifies factors associated with later steps of spliceosome assembly.Genetics · 2009Article
- Intronic alternative splicing regulators identified by comparative genomics in nematodes.PLoS computational biology · 2006Article
- Determinants of the inherent strength of human 5' splice sites.RNA (New York, N.Y.) · 2005Article
- Genetic suppression of intronic +1G mutations by compensatory U1 snRNA changes in Caenorhabditis elegans.Genetics · 2004Article
- Intrinsic differences between authentic and cryptic 5' splice sites.Nucleic acids research · 2003Article
- Analysis of the role of Caenorhabditis elegans GC-AG introns in regulated splicing.Nucleic acids research · 2002Article
- Genomic sequence, splicing, and gene annotation.American journal of human genetics · 2000Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in the Caenorhabditis elegans sup-39 gene cause allele-specific suppression of the uncoordination defect of unc-73(e936). e936 is a point mutation that changes the canonical G at the 5' end of intron 16 to a U. This mutation activates three splice donors, two of which define introns beginning with the canonical GU. Use of these two cryptic splice sites causes loss of reading frame; interestingly these messages are not substrates for nonsense-mediated decay. The third splice donor, used in 10% of steady-state e936 messages, is the mutated splice donor at the wild-type position, which defines an intron beginning with UU. In the presence of a sup-39 mutation, these same three splice donors are used, but the ratio of messages produced by splicing at these sites changes. The percentage of unc-73(e936) messages containing the wild-type splice junction is increased to 33% with a corresponding increase in the level of UNC-73 protein. This sup-39-induced change was also observed when the e936 mutant intron region was inserted into a heterologous splicing reporter construct transfected into worms. Experiments with splicing reporter constructs showed that the degree of 5' splice site match to the splicing consensus sequence can strongly influence cryptic splice site choice. We propose that mutant SUP-39 is a new type of informational suppressor that alters the use of weak splice donors.
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