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doi:10.1534/genetics.104.033894
A more recent version of this article appeared on April 1, 2005.
REGULAR RESEARCH PAPERS |
Roles of RAD6 epistasis group members in spontaneous Pol
-dependent translesion synthesis in Saccharomyces cerevisiae
Brenda K. Minesinger 1 and Sue Jinks-Robertson 1*
1 Emory University
* To whom correspondence should be addressed. E-mail: jinks{at}biology.emory.edu.
Submitted on July 23, 2004
Revised on August 30, 2004
Accepted on 10 January 2005
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 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
(zeta). In the current 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 required for Pol-dependent spontaneous mutagenesis in both error-prone pathways. A third, error-free pathway relies on the presence of Mms2, as well as Rad5 and Rad18. Examination of pol30-46 strains indicates that PCNA (POL30) has different roles in the error-free bypass of spontaneous versus induced damage.
Key Words: RAD6, polymerase zeta, spontaneous mutagenesis, translesion synthesis, yeast
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