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Mutagenesis Advance Access published online on November 9, 2009
Mutagenesis, doi:10.1093/mutage/gep045
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© The Author 2009. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

Roles of Rev1, Pol {zeta}, Pol32 and Pol {eta} in the bypass of chromosomal abasic sites in Saccharomyces cerevisiae

Paul A. Auerbach1 and Bruce Demple2,*

Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA 1Present address: Department of Molecular and Computational Biology, University of Southern California, Los Angeles, CA 90089, USA 2Present address: Department of Pharmacological Sciences, SBU Medical School, Basic Sciences Tower 8-140, Stony Brook, NY 11794, USA

Translesion synthesis (TLS) on DNA is a process by which potentially cytotoxic replication-blocking lesions are bypassed, but at the risk of increased mutagenesis. The exact in vivo role of the individual TLS enzymes in Saccharomyces cerevisiae has been difficult to determine from previous studies due to differing results from the variety of systems used. We have generated a series of S.cerevisiae strains in which each of the TLS-related genes REV1, REV3, REV7, RAD30 and POL32 was deleted, and in which chromosomal apyrimidinic sites were generated during normal cell growth by the activity of altered forms of human uracil-DNA glycosylase that remove undamaged cytosines or thymines. Deletion of REV1, REV3 or REV7 resulted in slower growth dependent on (rev3{Delta} and rev7{Delta}) or enhanced by (rev1{Delta}) expression of the mutator glycosylases and a nearly complete abolition of glycosylase-induced mutagenesis. Deletion of POL32 resulted in cell death when the mutator glycosylases were expressed and, in their absence, diminished spontaneous mutagenesis. RAD30 appeared to be unnecessary for mutagenesis in response to abasic sites, as deleting this gene caused no significant change in either the mutation rates or the mutational spectra due to glycosylase expression.

* To whom correspondence should be addressed. Tel. +1 631 444 3978; Fax +1 631 444 3218; Email: bruce{at}pharm.stonybrook.edu

Received on August 12, 2009; revised on September 11, 2009; accepted on September 23, 2009.


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