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Reference: Mudrak SV, et al. (2009) The polymerase {eta} translesion synthesis DNA polymerase acts independently of the mismatch repair system to limit mutagenesis caused by 7,8-dihydro-8-oxoguanine in yeast. Mol Cell Biol 29(19):5316-26

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Abstract

Reactive oxygen species are ubiquitous mutagens that have been linked to both disease and aging. The most studied oxidative lesion is 7,8-dihydro-8-oxoguanine (GO), which is often miscoded during DNA replication, resulting specifically in GC > TA transversions. In yeast, the mismatch repair (MMR) system repairs GO:A mismatches generated during DNA replication, and the Poleta translesion synthesis DNA polymerase additionally promotes error-free bypass of GO lesions. It has been suggested that Poleta limits GO-associated mutagenesis exclusively through its participation in the filling of MMR-generated gaps that contain GO lesions. In the experiments reported here, the SUP4-o forward mutation assay was used to monitor GC >TA mutation rates in strains defective in MMR (Msh2 or Msh6) and/or in Poleta activity. Results clearly demonstrate that Poleta can function independently of the MMR system to prevent GO-associated mutations, presumably through preferential insertion of cytosine opposite replication-blocking GO lesions. Furthermore, the Poleta-dependent bypass of GO lesions is more efficient on the lagging strand of replication and requires an interaction with PCNA. These studies establish a new paradigm for the prevention of GO-associated mutagenesis in eukaryotes.

Reference Type
Journal Article
Authors
Mudrak SV, Welz-Voegele C, Jinks-Robertson S
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