ArticleProceedings of the National Academy of Sciences of the United States of America2006
Inhibition of a spliceosome turnover pathway suppresses splicing defects.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 76 citations in OpenAlex.
- Structures of aberrant spliceosome intermediates on their way to disassembly.Nature structural & molecular biology · 2025Article
- Intron lariat spliceosomes convert lariats to true circles: implications for intron transposition.Genes & development · 2024Article
- Intron-lariat spliceosomes convert lariats to true circles: implications for intron transposition.bioRxiv : the preprint server for biology · 2024Article
- DHX15 is involved in SUGP1-mediated RNA missplicing by mutant SF3B1 in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
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- Auxiliary domains of the HrpB bacterial DExH-box helicase shape its RNA preferences.RNA biology · 2020Article
- Article
- Termination of pre-mRNA splicing requires that the ATPase and RNA unwindase Prp43p acts on the catalytic snRNA U6.Genes & development · 2019Article
- Cwc23 is a component of the NTR complex and functions to stabilize Ntr1 and facilitate disassembly of spliceosome intermediates.Nucleic acids research · 2018Article
- Regulation of Prp43-mediated disassembly of spliceosomes by its cofactors Ntr1 and Ntr2.Nucleic acids research · 2017Article
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- Article
- Functional roles of DExD/H-box RNA helicases in Pre-mRNA splicing.Journal of biomedical science · 2015Review
- Article
- NTR1 is required for transcription elongation checkpoints at alternative exons in Arabidopsis.The EMBO journal · 2015Article
- The G-patch protein Spp2 couples the spliceosome-stimulated ATPase activity of the DEAH-box protein Prp2 to catalytic activation of the spliceosome.Genes & development · 2015Article
- The DExD/H-box ATPase Prp2p destabilizes and proofreads the catalytic RNA core of the spliceosome.RNA (New York, N.Y.) · 2014Article
- Insights into the activation of the helicase Prp43 by biochemical studies and structural mass spectrometry.Nucleic acids research · 2014Article
- Splicing fidelity: DEAD/H-box ATPases as molecular clocks.RNA biology · 2013Review
- Structural basis for dual roles of Aar2p in U5 snRNP assembly.Genes & development · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Defects in assembly are suggested to signal the dissociation of faulty splicing complexes. A yeast genetic screen was performed to identify components of the putative discard pathway. Weak mutant alleles of SPP382 (also called NTR1) were found to suppress defects in two proteins required for spliceosome activation, Prp38p and Prp8p. Spp382p is shown necessary for cellular splicing, with premRNA and, for some alleles, excised intron, accumulating after inactivation. Like spp382-1, a mutant allele of AAR2 was identified in this suppressor screen. Like Spp382p, Aar2p has a reported role in spliceosome recycling and is found with Spp382p in a complex recovered with a mutant version of the spliceosomal core protein Prp8p. Possible insight into to the spp382 suppressor phenotype is provided by the observation that defective splicing complexes lacking the 5' exon cleavage intermediate are recovered by a tandem affinity purification-tagged Spp382 derivative. Stringent proteomic and two-hybrid analyses show that Spp382p also interacts with Cwc23p, a DNA J-like protein present in the spliceosome and copurified with the Prp43p DExD/H-box ATPase. Spp382p binds Prp43p and Prp43p requires Spp382p for intron release from the spliceosome. Consistent with a related function in the removal of defective complexes, three prp43 mutants are also shown to suppress splicing defects, with efficiencies inversely proportionate to the measured ATPase activities. These and related genetic data support the existence of a Spp382p-dependent turnover pathway acting on defective spliceosomes.
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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.