ArticleNucleic acids research2023
Splicing factor Prp18p promotes genome-wide fidelity of consensus 3'-splice sites.
Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Unraveling branch point-driven SR45a splicing dynamics in heat stress for plant adaptation.Science advances · 2026Article
- Splicing regulation and intron evolution in the short-intron ciliate model of endosymbiosis Paramecium bursaria.Nucleic acids research · 2026Article
- Control of 3' splice site selection inRNA (New York, N.Y.) · 2025Article
- The role of chimeric FAM72B transcripts generated by intergenic mRNA trans-splicing in breast cancer.Functional & integrative genomics · 2025Article
- Article
- Control of 3' splice site selection by the yeast splicing factor Fyv6.bioRxiv : the preprint server for biology · 2024Article
- Mechanisms and regulation of spliceosome-mediated pre-mRNA splicing in Saccharomyces cerevisiae.Wiley interdisciplinary reviews. RNAReview
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The fidelity of splice site selection is critical for proper gene expression. In particular, proper recognition of 3'-splice site (3'SS) sequences by the spliceosome is challenging considering the low complexity of the 3'SS consensus sequence YAG. Here, we show that absence of the Prp18p splicing factor results in genome-wide activation of alternative 3'SS in S. cerevisiae, including highly unusual non-YAG sequences. Usage of these non-canonical 3'SS in the absence of Prp18p is enhanced by upstream poly(U) tracts and by their potential to interact with the first intronic nucleoside, allowing them to dock in the spliceosome active site instead of the normal 3'SS. The role of Prp18p in 3'SS fidelity is facilitated by interactions with Slu7p and Prp8p, but cannot be fulfilled by Slu7p, identifying a unique role for Prp18p in 3'SS fidelity. This fidelity function is synergized by the downstream proofreading activity of the Prp22p helicase, but is independent from another late splicing helicase, Prp43p. Our results show that spliceosomes exhibit remarkably relaxed 3'SS sequence usage in the absence of Prp18p and identify a network of spliceosomal interactions centered on Prp18p which are required to promote the fidelity of the recognition of consensus 3'SS sequences.
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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.