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Originally published as Genetics Published Articles Ahead of Print on January 31, 2005.
Genetics, Vol. 169, 1939-1955, April 2005, Copyright © 2005
doi:10.1534/genetics.104.033894
Roles of RAD6 Epistasis Group Members in Spontaneous Pol
-Dependent Translesion Synthesis in Saccharomyces cerevisiae
Brenda K. Minesinger* and
Sue Jinks-Robertson*,
,1
* Biochemistry, Cell and Developmental Biology Program of the Graduate Division of Biological and Biomedical Sciences
Department of Biology, Emory University, Atlanta, Georgia 30322
1 Corresponding author: Department of Biology, Emory University, 1510 Clifton Rd., Atlanta, GA 30322.
E-mail: sue.jinks-robertson{at}emory.edu
DNA lesions that arise during normal cellular metabolism can block the progress of replicative DNA polymerases, leading to cell cycle arrest and, in higher eukaryotes, apoptosis. Alternatively, such blocking lesions can be temporarily tolerated using either a recombination- or a translesion synthesis-based bypass mechanism. In Saccharomyces cerevisiae, members of the RAD6 epistasis group are key players in the regulation of lesion bypass by the translesion DNA polymerase Pol
. In this study, changes in the reversion rate and spectrum of the lys2
A746 –1 frameshift allele have been used to evaluate how the loss of members of the RAD6 epistasis group affects Pol-dependent mutagenesis in response to spontaneous damage. Our data are consistent with a model in which Pol-dependent mutagenesis relies on the presence of either Rad5 or Rad18, which promote two distinct error-prone pathways that partially overlap with respect to lesion specificity. The smallest subunit of Pol
, Pol32, is also required for Pol-dependent spontaneous mutagenesis, suggesting a cooperative role between Pol and Pol for the bypass of spontaneous lesions. A third error-free pathway relies on the presence of Mms2, but may not require PCNA.
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