ArticleJournal of molecular biology2007
Saccharomyces cerevisiae MSH2-MSH3 and MSH2-MSH6 complexes display distinct requirements for DNA binding domain I in mismatch recognition.
Article in Journal of molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 54 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
- Msh2-Msh3 DNA-binding is not sufficient to promote trinucleotide repeat expansions in Saccharomyces cerevisiae.Genetics · 2025Article
- Tandem MutSβ binding to long extruded DNA trinucleotide repeats underpins pathogenic expansions.bioRxiv : the preprint server for biology · 2023Article
- Elevated MSH2 MSH3 expression interferes with DNA metabolism in vivo.Nucleic acids research · 2023Article
- Unexpected moves: a conformational change in MutSα enables high-affinity DNA mismatch binding.Nucleic acids research · 2023Article
- Conformational distortions induced by periodically recurring A…A in d(CAG).d(CAG) provide stereochemical rationale for the trapping of MSH2.MSH3 in polyQ disorders.Computational and structural biotechnology journal · 2021Article
- Coordination of Rad1-Rad10 interactions with Msh2-Msh3, Saw1 and RPA is essential for functional 3' non-homologous tail removal.Nucleic acids research · 2018Article
- Genomic Instability Promoted by Overexpression of Mismatch Repair Factors in Yeast: A Model for Understanding Cancer Progression.Genetics · 2018Article
- Article
- A MutSβ-Dependent Contribution of MutSα to Repeat Expansions in Fragile X Premutation Mice?PLoS genetics · 2016Article
- Oligonucleotide-directed mutagenesis screen to identify pathogenic Lynch syndrome-associated MSH2 DNA mismatch repair gene variants.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Dynamic DNA binding licenses a repair factor to bypass roadblocks in search of DNA lesions.Nature communications · 2016Article
- Article
- Activation of Saccharomyces cerevisiae Mlh1-Pms1 Endonuclease in a Reconstituted Mismatch Repair System.The Journal of biological chemistry · 2015Article
- Differential mismatch recognition specificities of eukaryotic MutS homologs, MutSα and MutSβ.Biophysical journal · 2014Article
- ATP binding and hydrolysis by Saccharomyces cerevisiae Msh2-Msh3 are differentially modulated by mismatch and double-strand break repair DNA substrates.DNA repair · 2014Article
- Mispair-specific recruitment of the Mlh1-Pms1 complex identifies repair substrates of the Saccharomyces cerevisiae Msh2-Msh3 complex.The Journal of biological chemistry · 2014Article
- Distinct requirements within the Msh3 nucleotide binding pocket for mismatch and double-strand break repair.Journal of molecular biology · 2013Article
- Genetic screens to identify pathogenic gene variants in the common cancer predisposition Lynch syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Postreplicative mismatch repair.Cold Spring Harbor perspectives in biology · 2013Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In eukaryotic mismatch repair (MMR) MSH2-MSH6 initiates the repair of base-base and small insertion/deletion mismatches while MSH2-MSH3 repairs larger insertion/deletion mismatches. Here, we show that the msh2Delta1 mutation, containing a complete deletion of the conserved mismatch recognition domain I of MSH2, conferred a separation of function phenotype with respect to MSH2-MSH3 and MSH2-MSH6 functions. Strains bearing the msh2Delta1 mutation were nearly wild-type in MSH2-MSH6-mediated MMR and in suppressing recombination between DNA sequences predicted to form mismatches recognized by MSH2-MSH6. However, these strains were completely defective in MSH2-MSH3-mediated MMR and recombination functions. This information encouraged us to analyze the contributions of domain I to the mismatch binding specificity of MSH2-MSH3 in genetic and biochemical assays. We found that domain I in MSH2 contributed a non-specific DNA binding activity while domain I of MSH3 appeared important for mismatch binding specificity and for suppressing non-specific DNA binding. These observations reveal distinct requirements for the MSH2 DNA binding domain I in the repair of DNA mismatches and suggest that the binding of MSH2-MSH3 to mismatch DNA involves protein-DNA contacts that appear very different from those required for MSH2-MSH6 mismatch binding.
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