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Originally published as Genetics Published Articles Ahead of Print on February 3, 2008.
Genetics, Vol. 178, 1221-1236, March 2008, Copyright © 2008
doi:10.1534/genetics.107.085415
Role of Proliferating Cell Nuclear Antigen Interactions in the Mismatch Repair-Dependent Processing of Mitotic and Meiotic Recombination Intermediates in Yeast
Jana E. Stone*,
,1,2,
Regan Gealy Ozbirn
,1,
Thomas D. Petes* and
Sue Jinks-Robertson*,3
* Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, Curriculum in Genetics and Molecular Biology, University of North Carolina, Chapel Hill, North Carolina 27599 and Graduate Division of Biological and Biomedical Sciences, Emory University, Atlanta, Georgia 30322
3 Corresponding author: Department of Molecular Genetics and Microbiology, DUMC 3020, 228 Jones Bldg., Research Dr., Durham, NC 27710.
E-mail: sue.robertson{at}duke.edu
The mismatch repair (MMR) system is critical not only for the repair of DNA replication errors, but also for the regulation of mitotic and meiotic recombination processes. In a manner analogous to its ability to remove replication errors, the MMR system can 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. In 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 mutations in the PCNA-encoding POL30 gene increase mutation rates in an 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 meiotic recombination. 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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Genetics 2008 178: NP.
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