ArticleMolecular and cellular biology2001
Repair of double-strand breaks by homologous recombination in mismatch repair-defective mammalian cells.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 174 citations in OpenAlex.
- Enhancing local meiotic crossovers in Arabidopsis and maize through juxtaposition of heterozygous and homozygous regions.Nature plants · 2025Article
- Homology-arm length of donor DNA affects the impact of Msh2 loss on homologous recombination-mediated gene targeting.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The decrease in Rad51 and DNA ligase IV nuclear protein expression in Msh2 knockdown HC11 cells induced the low CRISPR/Cas9-mediated knock-in efficiency at the β-casein gene locus.Animal bioscience · 2025Article
- The herpes simplex virus alkaline nuclease is required to maintain replication fork progression.Journal of virology · 2024Article
- Repetitive Sequence Stability in Embryonic Stem Cells.International journal of molecular sciences · 2024Review
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- MSH2 stimulates interfering and inhibits non-interfering crossovers in response to genetic polymorphism.Nature communications · 2023Article
- BRCA2 Germline Mutations Identify Gastric Cancers Responsive to PARP Inhibitors.Cancer research · 2023Article
- The effect of DNA polymorphisms and natural variation on crossover hotspot activity in Arabidopsis hybrids.Nature communications · 2023Article
- Multi-omics data integration analysis identifies the spliceosome as a key regulator of DNA double-strand break repair.NAR cancer · 2022Article
- Considerations for homology-based DNA repair in mosquitoes: Impact of sequence heterology and donor template source.PLoS genetics · 2022Article
- Relationship between DNA mismatch repair and CRISPR/Cas9-mediated knock-in in the bovine β-casein gene locus.Animal bioscience · 2022Article
- A Pan-Cancer Analysis on the Systematic Correlation of MutS Homolog 2 (MSH2) to a Malignant Tumor.Journal of oncology · 2022Article
- Single-Strand Annealing in Cancer.International journal of molecular sciences · 2021Review
- Factors enforcing the species boundary between the human pathogens Cryptococcus neoformans and Cryptococcus deneoformans.PLoS genetics · 2021Article
- Genetic evidence for the involvement of mismatch repair proteins, PMS2 and MLH3, in a late step of homologous recombination.The Journal of biological chemistry · 2020Article
- MSH2 shapes the meiotic crossover landscape in relation to interhomolog polymorphism in Arabidopsis.The EMBO journal · 2020Article
- Mechanistic Insight into Crossing over during Mouse Meiosis.Molecular cell · 2020Article
- A Genome-Wide Screen for Genes Affecting Spontaneous Direct-Repeat Recombination inG3 (Bethesda, Md.) · 2020Article
31 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chromosomal double-strand breaks (DSBs) stimulate homologous recombination by several orders of magnitude in mammalian cells, including murine embryonic stem (ES) cells, but the efficiency of recombination decreases as the heterology between the repair substrates increases (B. Elliott, C. Richardson, J. Winderbaum, J. A. Nickoloff, and M. Jasin, Mol. Cell. Biol. 18:93-101, 1998). We have now examined homologous recombination in mismatch repair (MMR)-defective ES cells to investigate both the frequency of recombination and the outcome of events. Using cells with a targeted mutation in the msh2 gene, we found that the barrier to recombination between diverged substrates is relaxed for both gene targeting and intrachromosomal recombination. Thus, substrates with 1.5% divergence are 10-fold more likely to undergo DSB-promoted recombination in Msh2(-/-) cells than in wild-type cells. Although mutant cells can repair DSBs efficiently, examination of gene conversion tracts in recombinants demonstrates that they cannot efficiently correct mismatched heteroduplex DNA (hDNA) that is formed adjacent to the DSB. As a result, >20-fold more of the recombinants derived from mutant cells have uncorrected tracts compared with recombinants from wild-type cells. The results indicate that gene conversion repair of DSBs in mammalian cells frequently involves mismatch correction of hDNA rather than double-strand gap formation. In cells with MMR defects, therefore, aberrant recombinational repair may be an additional mechanism that contributes to genomic instability and possibly tumorigenesis.
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