ArticleMolecular and cellular biology1998
Mismatch repair proteins regulate heteroduplex formation during mitotic recombination in yeast.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 110 citations in OpenAlex.
- Mechanisms That Govern Recombinase Fidelity Control During Eukaryotic Homologous Recombination.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Unveiling the mysteries of extrachromosomal circular DNA: from generation to clinical relevance in human cancers and health.Molecular cancer · 2024Review
- The herpes simplex virus alkaline nuclease is required to maintain replication fork progression.Journal of virology · 2024Article
- MSH2-MSH3 promotes DNA end resection during homologous recombination and blocks polymerase theta-mediated end-joining through interaction with SMARCAD1 and EXO1.Nucleic acids research · 2023Article
- Repair of mismatched templates during Rad51-dependent Break-Induced Replication.PLoS genetics · 2022Article
- Spectrum of DNA mismatch repair failures viewed through the lens of cancer genomics and implications for therapy.Clinical science (London, England : 1979) · 2022Article
- MicroDNA levels are dependent on MMEJ, repressed by c-NHEJ pathway, and stimulated by DNA damage.Nucleic acids research · 2021Article
- Collaborations between chromatin and nuclear architecture to optimize DNA repair fidelity.DNA repair · 2021Review
- Article
- Guidelines for DNA recombination and repair studies: Cellular assays of DNA repair pathways.Microbial cell (Graz, Austria) · 2019Review
- Genomic Instability Promoted by Overexpression of Mismatch Repair Factors in Yeast: A Model for Understanding Cancer Progression.Genetics · 2018Article
- A Distinct Class of Genome Rearrangements Driven by Heterologous Recombination.Molecular cell · 2018Article
- Article
- FANCJ helicase controls the balance between short- and long-tract gene conversions between sister chromatids.Nucleic acids research · 2017Article
- Understanding how mismatch repair proteins participate in the repair/anti-recombination decision.FEMS yeast research · 2016Article
- Article
- Genetic instability in budding and fission yeast-sources and mechanisms.FEMS microbiology reviews · 2015Review
- The Role of DNA Mismatch Repair and Recombination in the Processing of DNA Alkylating Damage in Living Yeast Cells.Advances in bioscience and biotechnology (Print) · 2015Article
- Frequent Interchromosomal Template Switches during Gene Conversion in S. cerevisiae.Molecular cell · 2014Article
- Modeling meiotic chromosomes indicates a size dependent contribution of telomere clustering and chromosome rigidity to homologue juxtaposition.PLoS computational biology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mismatch repair (MMR) proteins actively inhibit recombination between diverged sequences in both prokaryotes and eukaryotes. Although the molecular basis of the antirecombination activity exerted by MMR proteins is unclear, it presumably involves the recognition of mismatches present in heteroduplex recombination intermediates. This recognition could be exerted during the initial stage of strand exchange, during the extension of heteroduplex DNA, or during the resolution of recombination intermediates. We previously used an assay system based on 350-bp inverted-repeat substrates to demonstrate that MMR proteins strongly inhibit mitotic recombination between diverged sequences in Saccharomyces cerevisiae. The assay system detects only those events that reverse the orientation of the region between the recombination substrates, which can occur as a result of either intrachromatid crossover or sister chromatid conversion. In the present study we sequenced the products of mitotic recombination between 94%-identical substrates in order to map gene conversion tracts in wild-type versus MMR-defective yeast strains. The sequence data indicate that (i) most recombination occurs via sister chromatid conversion and (ii) gene conversion tracts in an MMR-defective strain are significantly longer than those in an isogenic wild-type strain. The shortening of conversion tracts observed in a wild-type strain relative to an MMR-defective strain suggests that at least part of the antirecombination activity of MMR proteins derives from the blockage of heteroduplex extension in the presence of mismatches.
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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.