ArticleGenes & development2015
A novel mechanism for Prp5 function in prespliceosome formation and proofreading the branch site sequence.
Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 82 citations in OpenAlex.
- Knockdown of the fly spliceosome component Rbp1 (orthologue of SRSF1) extends lifespan.GeroScience · 2026Article
- U2 snRNP recognizes the branch site through a loaded-spring strand-invasion mechanism.Nucleic acids research · 2026Article
- New mechanistic insights into prespliceosome formation-roles of DEAD-box proteins Prp5 and Sub2.RNA (New York, N.Y.) · 2025Article
- An RNA helicase coordinates with iron signal regulators to alleviate chilling stress in Arabidopsis.Nature communications · 2025Article
- Annotation and functional prediction of RNA helicases inIMA fungus · 2025Review
- Article
- Control of 3' splice site selection by the yeast splicing factor Fyv6.bioRxiv : the preprint server for biology · 2024Article
- Branch site recognition by the spliceosome.RNA (New York, N.Y.) · 2024Review
- Inefficient recruitment of DDX39B impedes pre-spliceosome assembly onRNA (New York, N.Y.) · 2024Article
- Structural insights into human exon-defined spliceosome prior to activation.Cell research · 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
- Splicing quality control mediated by DHX15 and its G-patch activator SUGP1.Cell reports · 2023Article
- Cellular functions of eukaryotic RNA helicases and their links to human diseases.Nature reviews. Molecular cell biology · 2023Review
- Genome-scale mapping of DNA damage suppressors through phenotypic CRISPR-Cas9 screens.Molecular cell · 2023Article
- Mechanisms of the RNA helicases DDX42 and DDX46 in human U2 snRNP assembly.Nature communications · 2023Article
- Structural studies of the spliceosome: Bridging the gaps.Current opinion in structural biology · 2022Review
- A model for DHX15 mediated disassembly of A-complex spliceosomes.RNA (New York, N.Y.) · 2022Article
- Structural basis of branch site recognition by the human spliceosome.Science (New York, N.Y.) · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The DEAD-box RNA helicase Prp5 is required for the formation of the prespliceosome through an ATP-dependent function to remodel U2 small nuclear ribonucleoprotein particles (snRNPs) and an ATP-independent function of unknown mechanism. Prp5 has also been implicated in proofreading the branch site sequence, but the molecular mechanism has not been well characterized. Using actin precursor mRNA (pre-mRNA) carrying branch site mutations, we identified a Prp5-containing prespliceosome with Prp5 directly bound to U2 small nuclear RNA (snRNA). Prp5 is in contact with U2 in regions on and near the branchpoint-interacting stem-loop (BSL), suggesting that Prp5 may function in stabilizing the BSL. Regardless of its ATPase activity, Prp5 mutants that suppress branch site mutations associate with the spliceosome less tightly and allow more tri-snRNP binding for the reaction to proceed. Our results suggest a novel mechanism for how Prp5 functions in prespliceosome formation and proofreading of the branch site sequence. Prp5 binds to the spliceosome in association with U2 by interacting with the BSL and is released upon the base-pairing of U2 with the branch site to allow the recruitment of the tri-snRNP. Mutations impairing U2-branch site base-pairing retard Prp5 release and impede tri-snRNP association. Prp5 mutations that destabilize the Prp5-U2 interaction suppress branch site mutations by allowing progression of the pathway.
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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.