ArticleGenetics2001
Requirement for Msh6, but not for Swi4 (Msh3), in Msh2-dependent repair of base-base mismatches and mononucleotide loops in Schizosaccharomyces pombe.
Article in Genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- DNA Repair in Haploid Context.International journal of molecular sciences · 2021Review
- A mutated dph3 gene causes sensitivity of Schizosaccharomyces pombe cells to cytotoxic agents.Current genetics · 2017Article
- Article
- Preferential Protection of Genetic Fidelity within Open Chromatin by the Mismatch Repair Machinery.The Journal of biological chemistry · 2016Article
- Meiotic Recombination in Schizosaccharomyces pombe: A Paradigm for Genetic and Molecular Analysis.Genome dynamics and stability · 2008Article
- Schizosaccharomyces pombe switches mating type by the synthesis-dependent strand-annealing mechanism.Genetics · 2007Article
- The role of DNA mismatch repair in generating genetic diversity and drug resistance in malaria parasites.Molecular and biochemical parasitology · 2007Article
- Stripped-down DNA repair in a highly reduced parasite.BMC molecular biology · 2007Article
- Mutation rates, spectra and hotspots in mismatch repair-deficient Caenorhabditis elegans.Genetics · 2005Article
- Repair of damaged and mismatched DNA by the XPC homologues Rhp41 and Rhp42 of fission yeast.Genetics · 2003Article
- Control of GT repeat stability in Schizosaccharomyces pombe by mismatch repair factors.Genetics · 2001Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The msh6 mismatch repair gene of Schizosaccharomyces pombe was cloned, sequenced, and inactivated. Strains bearing all combinations of inactivated msh6, msh2, and swi4 (the S. pombe MSH3 ortholog) alleles were tested for their defects in mitotic and meiotic mismatch repair. Mitotic mutation rates were similarly increased in msh6 and msh2 mutants, both for reversion of a base-base substitution as well as of an insertion of one nucleotide in a mononucleotide run. Tetrad analysis and intragenic two-factor crosses revealed that meiotic mismatch repair was affected in msh6 to the same extent as in msh2 background. In contrast, loss of Swi4 likely did not cause a defect in mismatch repair, but rather resulted in reduced recombination frequency. Consistently, a mutated swi4 caused a two- to threefold reduction of recombinants in intergenic crosses, while msh2 and msh6 mutants were not significantly different from wild type. In summary, our study showed that Msh6 plays the same important role as Msh2 in the major mismatch repair pathway of S. pombe, while Swi4 rather functions in recombination.
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Registered trials
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.