ArticleNature structural & molecular biology2006
Exon ligation is proofread by the DExD/H-box ATPase Prp22p.
Article in Nature structural & molecular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
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Who cites it
103 citing papers in PubMed.
- Fragment-Based Discovery of Potent RNA-Competitive Inhibitors of the DEAH-Box RNA Helicase DHX8.Journal of medicinal chemistry · 2026Article
- REAL-TIME VISUALIZATION OF SPLICEOSOME ASSEMBLY REVEALS BASIC PRINCIPLES OF 3' SPLICE SITE SELECTION.Research square · 2026Article
- Structural basis of the regulation by CDK11 kinase of early spliceosome activation and evidence for its proofreading by DHX15 helicase.Nature communications · 2026Article
- Human DEAH-box helicase 8 regulates HSF1-mediated stress response and cancer-associated pre-mRNA splicing in tumour cells.NAR cancer · 2026Article
- Article
- Control of 3' splice site selection inRNA (New York, N.Y.) · 2025Article
- Unraveling gene expression: a beginner's guide from chromatin modifications to mRNA export inNucleus (Austin, Tex.) · 2025Review
- New mechanistic insights into Prp22-mediated exon ligation and mRNA release.Nucleic acids research · 2025Article
- Structures of aberrant spliceosome intermediates on their way to disassembly.Nature structural & molecular biology · 2025Article
- Dynamics and evolutionary conservation of B complex protein recruitment during spliceosome activation.Nucleic acids research · 2025Article
- Article
- Control of 3' splice site selection by the yeast splicing factor Fyv6.bioRxiv : the preprint server for biology · 2024Article
- Dynamics and Evolutionary Conservation of B Complex Protein Recruitment During Spliceosome Activation.bioRxiv : the preprint server for biology · 2024Article
- Spliceosomal helicases DDX41/SACY-1 and PRP22/MOG-5 both contribute to proofreading against proximal 3' splice site usage.RNA (New York, N.Y.) · 2024Article
- 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
- Targeted high-throughput mutagenesis of the human spliceosome reveals its in vivo operating principles.Molecular cell · 2023Article
- XAP5 CIRCADIAN TIMEKEEPER regulates RNA splicing and the circadian clock by genetically separable pathways.Plant physiology · 2023Article
- Regulation of 3' splice site selection after step 1 of splicing by spliceosomal C* proteins.Science advances · 2023Article
- Yeast U6 snRNA made by RNA polymerase II is less stable but functional.RNA (New York, N.Y.) · 2022Article
43 more citing papers are in PubMed but not listed here.
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Abstract
To produce messenger RNA, the spliceosome excises introns from precursor (pre)-mRNA and splices the flanking exons. To establish fidelity, the spliceosome discriminates against aberrant introns, but current understanding of such fidelity mechanisms is limited. Here we show that an ATP-dependent activity represses formation of mRNA from aberrant intermediates having mutations in any of the intronic consensus sequences. This proofreading activity is disabled by mutations that impair the ATPase or RNA unwindase activity of Prp22p, a conserved spliceosomal DExD/H-box ATPase. Further, cold-sensitive prp22 mutants permit aberrant mRNA formation from a mutated 3' splice-site intermediate in vivo. We conclude that Prp22p generally represses splicing of aberrant intermediates, in addition to its known ATP-dependent role in promoting release of genuine mRNA. This dual function for Prp22p validates a general model in which fidelity can be enhanced by a DExD/H-box ATPase.
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