ArticlePLoS genetics2013
Different roles of eukaryotic MutS and MutL complexes in repair of small insertion and deletion loops in yeast.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Mismatch repair MLH complexes make distinct contributions to post-replicative mismatch repair versus trinucleotide repeat expansions.bioRxiv : the preprint server for biology · 2026Article
- Aspergillus fumigatus mitogenomes and their influence on azole-resistant and -susceptible populations.npj antimicrobials and resistance · 2025Article
- Elevated mutation rates in multi-azole resistant Aspergillus fumigatus drive rapid evolution of antifungal resistance.Nature communications · 2024Article
- Instability throughout the Saccharomyces cerevisiae genome resulting from Pms1 endonuclease deficiency.Nucleic acids research · 2024Article
- The mismatch repair endonuclease MutLα tethers duplex regions of DNA together and relieves DNA torsional tension.Nucleic acids research · 2023Article
- Article
- Multiple Losses of MSH1, Gain of mtMutS, and Other Changes in the MutS Family of DNA Repair Proteins in Animals.Genome biology and evolution · 2021Article
- Experimental exchange of paralogous domains in the MLH family provides evidence of sub-functionalization after gene duplication.G3 (Bethesda, Md.) · 2021Article
- Review
- High-fidelity DNA ligation enforces accurate Okazaki fragment maturation during DNA replication.Nature communications · 2021Article
- Expanded roles for the MutL family of DNA mismatch repair proteins.Yeast (Chichester, England) · 2021Review
- Transcription-coupled repair and mismatch repair contribute towards preserving genome integrity at mononucleotide repeat tracts.Nature communications · 2020Article
- R-loops: targets for nuclease cleavage and repeat instability.Current genetics · 2018Review
- Cytosine deamination and base excision repair cause R-loop-induced CAG repeat fragility and instability inProceedings of the National Academy of Sciences of the United States of America · 2017Article
- mlh3 mutations in baker's yeast alter meiotic recombination outcomes by increasing noncrossover events genome-wide.PLoS genetics · 2017Article
- The mismatch repair and meiotic recombination endonuclease Mlh1-Mlh3 is activated by polymer formation and can cleave DNA substrates in trans.PLoS biology · 2017Article
- Preferential Protection of Genetic Fidelity within Open Chromatin by the Mismatch Repair Machinery.The Journal of biological chemistry · 2016Article
- Absence of MutSβ leads to the formation of slipped-DNA for CTG/CAG contractions at primate replication forks.DNA repair · 2016Article
- Non-canonical actions of mismatch repair.DNA repair · 2016Review
- Genetic instability in budding and fission yeast-sources and mechanisms.FEMS microbiology reviews · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA mismatch repair greatly increases genome fidelity by recognizing and removing replication errors. In order to understand how this fidelity is maintained, it is important to uncover the relative specificities of the different components of mismatch repair. There are two major mispair recognition complexes in eukaryotes that are homologues of bacterial MutS proteins, MutSα and MutSβ, with MutSα recognizing base-base mismatches and small loop mispairs and MutSβ recognizing larger loop mispairs. Upon recognition of a mispair, the MutS complexes then interact with homologues of the bacterial MutL protein. Loops formed on the primer strand during replication lead to insertion mutations, whereas loops on the template strand lead to deletions. We show here in yeast, using oligonucleotide transformation, that MutSα has a strong bias toward repair of insertion loops, while MutSβ has an even stronger bias toward repair of deletion loops. Our results suggest that this bias in repair is due to the different interactions of the MutS complexes with the MutL complexes. Two mutants of MutLα, pms1-G882E and pms1-H888R, repair deletion mispairs but not insertion mispairs. Moreover, we find that a different MutL complex, MutLγ, is extremely important, but not sufficient, for deletion repair in the presence of either MutLα mutation. MutSβ is present in many eukaryotic organisms, but not in prokaryotes. We suggest that the biased repair of deletion mispairs may reflect a critical eukaryotic function of MutSβ in mismatch repair.
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