ArticleProceedings of the National Academy of Sciences of the United States of America2010
Spliceosome discards intermediates via the DEAH box ATPase Prp43p.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed.
- REAL-TIME VISUALIZATION OF SPLICEOSOME ASSEMBLY REVEALS BASIC PRINCIPLES OF 3' SPLICE SITE SELECTION.Research square · 2026Article
- GPATCH11 ortholog Sap34 regulates pre-mRNA splicing by interacting with early spliceosomal complexes in Schizosaccharomyces pombe.Scientific reports · 2026Article
- Coordinated alternative splicing decisions via stepwise exon definition.Nucleic acids research · 2026Article
- Structures of aberrant spliceosome intermediates on their way to disassembly.Nature structural & molecular biology · 2025Article
- Structural insights into spliceosome fidelity: DHX35-GPATCH1- mediated rejection of aberrant splicing substrates.Cell research · 2025Article
- Splicing factor Prp18p promotes genome-wide fidelity of consensus 3'-splice sites.Nucleic acids research · 2023Article
- An ATP-independent role for Prp16 in promoting aberrant splicing.Nucleic acids research · 2023Article
- Splicing quality control mediated by DHX15 and its G-patch activator SUGP1.Cell reports · 2023Article
- Targeted high-throughput mutagenesis of the human spliceosome reveals its in vivo operating principles.Molecular cell · 2023Article
- Conformational dynamics of the RNA binding channel regulates loading and translocation of the DEAH-box helicase Prp43.Nucleic acids research · 2023Article
- CircRNF10-DHX15 interaction suppressed breast cancer progression by antagonizing DHX15-NF-κB p65 positive feedback loop.Cellular & molecular biology letters · 2023Article
- Regulation of the DEAH/RHA helicase Prp43 by the G-patch factor Pfa1.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Alternative splicing regulation of cell-cycle genes by SPF45/SR140/CHERP complex controls cell proliferation.RNA (New York, N.Y.) · 2021Article
- The G-patch activators Pfa1 and PINX1 exhibit different modes of interaction with the Prp43 RNA helicase.RNA biology · 2021Article
- psiCLIP reveals dynamic RNA binding by DEAH-box helicases before and after exon ligation.Nature communications · 2021Article
- Structural basis for DEAH-helicase activation by G-patch proteins.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The inactive C-terminal cassette of the dual-cassette RNA helicase BRR2 both stimulates and inhibits the activity of the N-terminal helicase unit.The Journal of biological chemistry · 2020Article
- Termination of pre-mRNA splicing requires that the ATPase and RNA unwindase Prp43p acts on the catalytic snRNA U6.Genes & development · 2019Article
- Structural and functional modularity of the U2 snRNP in pre-mRNA splicing.Critical reviews in biochemistry and molecular biology · 2019Review
- Structural Basis of Nuclear pre-mRNA Splicing: Lessons from Yeast.Cold Spring Harbor perspectives in biology · 2019Review
5 more citing papers are in PubMed but not listed here.
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4 authors.
Funding
Abstract
To promote fidelity in nuclear pre-mRNA splicing, the spliceosome rejects and discards suboptimal substrates that have engaged the spliceosome. Whereas DExD/H box ATPases have been implicated in rejecting suboptimal substrates, the mechanism for discarding suboptimal substrates has remained obscure. Corroborating evidence that suboptimal, mutated lariat intermediates can be exported to the cytoplasm for turnover, we have found that the ribosome can translate mutated lariat intermediates. By glycerol gradient analysis, we have found that the spliceosome can dissociate mutated lariat intermediates in vivo in a manner that requires the DEAH box ATPase Prp43p. Through an in vitro assay, we demonstrate that Prp43p promotes the discard of suboptimal and optimal 5' exon and lariat intermediates indiscriminately. Finally, we demonstrate a requirement for Prp43p in repressing splicing at a cryptic splice site. We propose a model for the fidelity of exon ligation in which the DEAH box ATPase Prp22p slows the flow of suboptimal intermediates through exon ligation and Prp43p generally promotes discard of intermediates, thereby establishing a pathway for turnover of stalled intermediates. Because Prp43p also promotes spliceosome disassembly after exon ligation, this work establishes a parallel between the discard of suboptimal intermediates and the dissociation of a genuine excised intron product.
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