ArticleGenetics2004
Yeast MPH1 gene functions in an error-free DNA damage bypass pathway that requires genes from Homologous recombination, but not from postreplicative repair.
Article in Genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.
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Who cites it
61 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Distinct repair processes produce APOBEC-induced deletions, tandem substitutions, and complex mutations in yeast and human cells.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Highly mutagenic copying of telomeric circles promotes ALT establishment.Nature communications · 2026Article
- Recurrent DNA nicks drive massive expansions of (GAA)Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- High-throughput screening of the Saccharomyces cerevisiae genome for 2-amino-3-methylimidazo [4,5-f] quinoline resistance identifies colon cancer-associated genes.G3 (Bethesda, Md.) · 2023Article
- Review
- Repair of base damage within break-induced replication intermediates promotes kataegis associated with chromosome rearrangements.Nucleic acids research · 2019Article
- Article
- The Smc5/6 complex regulates the yeast Mph1 helicase at RNA-DNA hybrid-mediated DNA damage.PLoS genetics · 2017Article
- Srs2 promotes synthesis-dependent strand annealing by disrupting DNA polymerase δ-extending D-loops.eLife · 2017Article
- Avoidance of APOBEC3B-induced mutation by error-free lesion bypass.Nucleic acids research · 2017Article
- Hypermutation signature reveals a slippage and realignment model of translesion synthesis by Rev3 polymerase in cisplatin-treated yeast.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Histone H2B mono-ubiquitylation maintains genomic integrity at stalled replication forks.Nucleic acids research · 2016Article
- Dosage Mutator Genes in Saccharomyces cerevisiae: A Novel Mutator Mode-of-Action of the Mph1 DNA Helicase.Genetics · 2016Article
- Binding of the Fkh1 Forkhead Associated Domain to a Phosphopeptide within the Mph1 DNA Helicase Regulates Mating-Type Switching in Budding Yeast.PLoS genetics · 2016Article
- Article
- MTE1 Functions with MPH1 in Double-Strand Break Repair.Genetics · 2016Article
- Mutation at a distance caused by homopolymeric guanine repeats in Saccharomyces cerevisiae.Science advances · 2016Article
- Differential regulation of the anti-crossover and replication fork regression activities of Mph1 by Mte1.Genes & development · 2016Article
- Mte1 interacts with Mph1 and promotes crossover recombination and telomere maintenance.Genes & development · 2016Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MPH1 gene from Saccharomyces cerevisiae, encoding a member of the DEAH family of proteins, had been identified by virtue of the spontaneous mutator phenotype of respective deletion mutants. Genetic analysis suggested that MPH1 functions in a previously uncharacterized DNA repair pathway that protects the cells from damage-induced mutations. We have now analyzed genetic interactions of mph1 with a variety of mutants from different repair systems with respect to spontaneous mutation rates and sensitivities to different DNA-damaging agents. The dependence of the mph1 mutator phenotype on REV3 and REV1 and the synergy with mutations in base and nucleotide excision repair suggest an involvement of MPH1 in error-free bypass of lesions. However, although we observed an unexpected partial suppression of the mph1 mutator phenotype by rad5, genetic interactions with other mutations in postreplicative repair imply that MPH1 does not belong to this pathway. Instead, mutations from the homologous recombination pathway were found to be epistatic to mph1 with respect to both spontaneous mutation rates and damage sensitivities. Determination of spontaneous mitotic recombination rates demonstrated that mph1 mutants are not deficient in homologous recombination. On the contrary, in an sgs1 background we found a pronounced hyperrecombination phenotype. Thus, we propose that MPH1 is involved in a branch of homologous recombination that is specifically dedicated to error-free bypass.
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