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Ribonucleotides are signals for mismatch repair of leading-strand replication errors.

Journal article
Authors Scott A Lujan
Jessica S Williams
Anders R Clausen
Alan B Clark
Thomas A Kunkel
Published in Molecular cell
Volume 50
Issue 3
Pages 437-43
ISSN 1097-4164
Publication year 2013
Published at
Pages 437-43
Language en
Links dx.doi.org/10.1016/j.molcel.2013.03...
www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords DNA Mismatch Repair, DNA Polymerase II, genetics, metabolism, DNA Polymerase III, genetics, metabolism, DNA Replication, genetics, Genomic Instability, Ribonuclease H, genetics, metabolism, Ribonucleotides, genetics, metabolism, Saccharomyces cerevisiae, enzymology, genetics, metabolism, Saccharomyces cerevisiae Proteins, genetics, metabolism
Subject categories Molecular biology, Genetics

Abstract

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 ε as compared to lagging-strand DNA polymerase δ. 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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