期刊
MOLECULAR CELL
卷 50, 期 3, 页码 437-443出版社
CELL PRESS
DOI: 10.1016/j.molcel.2013.03.017
关键词
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资金
- Division of Intramural Research of the National Institutes of Health [Z01 ES065070]
- National Institute of Environmental Health Sciences
To maintain genome stability, mismatch repair of nuclear DNA replication errors must be directed to the nascent strand, likely by DNA ends and PCNA. Here we show that the efficiency of mismatch repair in Saccharomyces cerevisiae is reduced by inactivating RNase H2, which nicks DNA containing ribonucleotides incorporated during replication. In strains encoding mutator polymerases, this reduction is preferential for repair of mismatches made by leading-strand DNA polymerase epsilon as compared to lagging-strand DNA polymerase delta. The results suggest that RNase-H2-dependent processing of ribonucleotides transiently present in DNA after replication may direct mismatch repair to the continuously replicated nascent leading strand.
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