Journal
GENETICS
Volume 178, Issue 3, Pages 1221-1236Publisher
GENETICS SOCIETY AMERICA
DOI: 10.1534/genetics.107.085415
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Funding
- NIGMS NIH HHS [T32 GM007092, R01 GM024110, GM-07092, R01 GM038464, GM-038464, GM-024110] Funding Source: Medline
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The mismatch repair (MMR) system is critical not only for the repair of DNA replication errors, hilt also for the regulation of mitotic and meiotic recombination processes. In a manner analogous to its ability to remove replication errors, the MMR system call remove mismatches in heteroduplex recombination intermediates to generate gene conversion events. Alternatively, such mismatches can trigger an MMR-dependent antirecombination activity that blocks the completion of recombination, thereby limiting interactions between diverged sequences. lit Saccharomyces cerevisiae, the MMR proteins Msh3, Msh6, and Mlh1 interact with proliferating cell nuclear antigen (PCNA), and mutations that. disrupt, these interactions result in a mutator phenotype. In addition, some initiations in the PCNA-encoding POL30 gene increase mutation rates in all MMR-dependent manner. In the current study, pol30, mlh1, and msh6 mutants were used to examine whether MMR-PCNA interactions are similarly important during mitotic and mitotic re-combination. We find that MMR-PCNA interactions are important. for repairing mismatches formed during meiotic recombination, but play only a relatively minor role in regulating the fidelity of mitotic recombination.
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