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The mismatch repair system promotes DNA polymerase ζ-dependent translesion synthesis in yeast

By Kevin Lehner and Sue Jinks-Robertson


DNA lesions that block replication can be bypassed by error-prone or error-free mechanisms. Error-prone mechanisms rely on specialized translesion synthesis (TLS) DNA polymerases that directly replicate over the lesion, whereas error-free pathways use an undamaged duplex as a template for lesion bypass. In the yeast Saccharomyces cerevisiae, most mutagenic TLS of spontaneous and induced DNA damage relies on DNA polymerase ζ (Polζ) activity. Here, we use a distinct mutational signature produced by Polζ in a frameshift-reversion assay to examine the role of the yeast mismatch repair (MMR) system in regulating Polζ-dependent mutagenesis. Whereas MMR normally reduces mutagenesis by removing errors introduced by replicative DNA polymerases, we find that the MMR system is required for Polζ-dependent mutagenesis. In the absence of homologous recombination, however, the error-prone Polζ pathway is not affected by MMR status. These results demonstrate that MMR promotes Polζ-dependent mutagenesis by inhibiting an alternative, error-free pathway that depends on homologous recombination. Finally, in contrast to its ability to remove mistakes made by replicative DNA polymerases, we show that MMR fails to efficiently correct errors introduced by Polζ

Topics: Biological Sciences
Publisher: National Academy of Sciences
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Provided by: PubMed Central
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