Journal
MOLECULAR CELL
Volume 50, Issue 3, Pages 437-443Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2013.03.017
Keywords
-
Categories
Funding
- Division of Intramural Research of the National Institutes of Health [Z01 ES065070]
- National Institute of Environmental Health Sciences
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available