ArticleRNA (New York, N.Y.)2000
Dominant negative mutants of the yeast splicing factor Prp2 map to a putative cleft region in the helicase domain of DExD/H-box proteins.
Article in RNA (New York, N.Y.), 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- The RNA helicase DHX16 recognizes specific viral RNA to trigger RIG-I-dependent innate antiviral immunity.Cell reports · 2022Article
- Conserved motifs in the flavivirus NS3 RNA helicase enzyme.Wiley interdisciplinary reviews. RNA · 2022Review
- Termination of pre-mRNA splicing requires that the ATPase and RNA unwindase Prp43p acts on the catalytic snRNA U6.Genes & development · 2019Article
- Structural toggle in the RNaseH domain of Prp8 helps balance splicing fidelity and catalytic efficiency.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Single-Molecule Pull-Down FRET to Dissect the Mechanisms of Biomolecular Machines.Methods in enzymology · 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
- GPKOW is essential for pre-mRNA splicing in vitro and suppresses splicing defect caused by dominant-negative DHX16 mutation in vivo.Bioscience reports · 2014Article
- The DExD/H-box ATPase Prp2p destabilizes and proofreads the catalytic RNA core of the spliceosome.RNA (New York, N.Y.) · 2014Article
- Biased Brownian ratcheting leads to pre-mRNA remodeling and capture prior to first-step splicing.Nature structural & molecular biology · 2013Article
- The interaction of Prp2 with a defined region of the intron is required for the first splicing reaction.Molecular and cellular biology · 2012Article
- Contribution of DEAH-box protein DHX16 in human pre-mRNA splicing.The Biochemical journal · 2010Article
- Release of SF3 from the intron branchpoint activates the first step of pre-mRNA splicing.RNA (New York, N.Y.) · 2010Article
- Translation initiation factor 4A: a prototype member of dead-box protein family.Physiology and molecular biology of plants : an international journal of functional plant biology · 2008Article
- A novel splicing factor, Yju2, is associated with NTC and acts after Prp2 in promoting the first catalytic reaction of pre-mRNA splicing.Molecular and cellular biology · 2007Article
- Mutations in PRP43 that uncouple RNA-dependent NTPase activity and pre-mRNA splicing function.Biochemistry · 2006Article
- Comprehensive mutational analysis of yeast DEXD/H box RNA helicases required for small ribosomal subunit synthesis.Molecular and cellular biology · 2006Article
- Characterization of the ATPase and unwinding activities of the yeast DEAD-box protein Has1p and the analysis of the roles of the conserved motifs.Nucleic acids research · 2005Article
- Interaction between a G-patch protein and a spliceosomal DEXD/H-box ATPase that is critical for splicing.Molecular and cellular biology · 2004Article
- Definition of a spliceosome interaction domain in yeast Prp2 ATPase.RNA (New York, N.Y.) · 2004Article
- Structure-based mutational analysis of the hepatitis C virus NS3 helicase.Journal of virology · 2001Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The Prp2 protein of Saccharomyces cerevisiae is an RNA-dependent ATPase required before the first transesterification reaction in pre-mRNA splicing. Prp2 binds to the spliceosome in the absence of ATP and is released following ATP hydrolysis. We determined what regions in Prp2 are essential for release from the spliceosome by analyzing dominant negative mutants in vivo and in vitro. We made mutations in conserved motif II (DExH) and motif VI (QRxGR) of the helicase (H) domain. Mutations that inactivated PRP2 had a dominant negative phenotype when overexpressed in vivo. To test whether mutations outside of the H domain could confer a dominant negative phenotype, we mutagenized a GAL1-PRP2 construct and screened for mutants unable to grow on galactose-containing media. Five dominant negative mutants were characterized; three mapped within the H domain and two mapped downstream of motif VI, indicating that an extended helicase domain is required for release of Prp2 from the spliceosome. Most mutants stalled in the spliceosome in vitro. However, not all mutants that were dominant negative in vivo were dominant negative in vitro, indicating that multiple mechanisms may cause a dominant negative phenotype. Structural modeling of the H domain of Prp2 suggests that mutants map to a cleft region found in helicases of known structure.
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