ArticleNucleic acids research2021
Evidence for complex dynamics during U2 snRNP selection of the intron branchpoint.
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 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- U2 snRNP recognizes the branch site through a loaded-spring strand-invasion mechanism.Nucleic acids research · 2026Article
- Unraveling branch point-driven SR45a splicing dynamics in heat stress for plant adaptation.Science advances · 2026Article
- New mechanistic insights into prespliceosome formation-roles of DEAD-box proteins Prp5 and Sub2.RNA (New York, N.Y.) · 2025Article
- PROTEIN PHOSPHATASE 2A B'η drives spliceosome subunit dephosphorylation to mediate alternative splicing following heat stress.The Plant cell · 2025Article
- Alternative Splicing: A Critical Regulator in Human Bone Biology and Tumor Progression.Research (Washington, D.C.) · 2025Review
- KHSRP ameliorates acute liver failure by regulating pre-mRNA splicing through its interaction with SF3B1.Cell death & disease · 2024Article
- Structural insights into branch site proofreading by human spliceosome.Nature structural & molecular biology · 2024Article
- Broad variation in response of individual introns to splicing inhibitors in a humanized yeast strain.RNA (New York, N.Y.) · 2024Article
- Broad variation in response of individual introns to splicing inhibitors in a humanized yeast strain.bioRxiv : the preprint server for biology · 2023Article
- An ATP-independent role for Prp16 in promoting aberrant splicing.Nucleic acids research · 2023Article
- Biochemical and genetic evidence supports Fyv6 as a second-step splicing factor inRNA (New York, N.Y.) · 2023Article
- Structural basis of branch site recognition by the human spliceosome.Science (New York, N.Y.) · 2022Article
- Attacking a DEAD problem: The role of DEAD-box ATPases in ribosome assembly and beyond.Methods in enzymology · 2022Article
- Mechanisms and regulation of spliceosome-mediated pre-mRNA splicing in Saccharomyces cerevisiae.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Splicing of pre-mRNA is initiated by binding of U1 to the 5' splice site and of Msl5-Mud2 heterodimer to the branch site (BS). Subsequent binding of U2 displaces Msl5-Mud2 from the BS to form the prespliceosome, a step governing branchpoint selection and hence 3' splice site choice, and linking splicing to myelodysplasia and many cancers in human. Two DEAD-box proteins, Prp5 and Sub2, are required for this step, but neither is stably associated with the pre-mRNA during the reaction. Using BS-mutated ACT1 pre-mRNA, we previously identified a splicing intermediate complex, FIC, which contains U2 and Prp5, but cannot bind the tri-snRNP. We show here that Msl5 remains associated with the upstream cryptic branch site (CBS) in the FIC, with U2 binding a few bases downstream of the BS. U2 mutants that restore U2-BS base pairing enable dissociation of Prp5 and allows splicing to proceed. The CBS is required for splicing rescue by compensatory U2 mutants, and for formation of FIC, demonstrating a role for Msl5 in directing U2 to the BS, and of U2-BS base pairing for release of Prp5 and Msl5-Mud2 to form the prespliceosome. Our results provide insights into how the prespliceosome may form in normal splicing reaction.
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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.