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Nucleic Acids Research 2004 32(12):3712-3723; doi:10.1093/nar/gkh696
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Published online 14 July 2004

Nucleic Acids Research, Vol. 32 No. 12 © Oxford University Press 2004; all rights reserved

Biological consequences of oxidative stress-induced DNA damage in Saccharomyces cerevisiae

Tiffany B. Salmon1,2, Barbara A. Evert1,2, Binwei Song1 and Paul W. Doetsch3,*

1 Department of Biochemistry, 2 Graduate Program in Genetics and Molecular Biology and 3 Department of Biochemistry and Division of Cancer Biology and Department of Radiation Oncology, Emory University School of Medicine, Atlanta, GA 30322, USA

* To whom correspondence should be addressed. Tel: +1 404 727 0409; Fax: +1 404 727 2618; Email: medpwd{at}emory.edu
The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors

Received April 30, 2004; Revised June 11, 2004; Accepted June 21, 2004

Reactive oxygen species (ROS), generated by endogenous and exogenous sources, cause significant damage to macromolecules, including DNA. To determine the cellular effects of induced, oxidative DNA damage, we established a relationship between specific oxidative DNA damage levels and biological consequences produced by acute H2O2 exposures in yeast strains defective in one or two DNA damage-handling pathways. We observed that unrepaired, spontaneous DNA damage interferes with the normal cellular response to exogenous oxidative stress. In addition, when base excision repair (BER) is compromised, there is a preference for using recombination (REC) over translesion synthesis (TLS) for handling H2O2-induced DNA damage. The global genome transcriptional response of these strains to exogenous H2O2 exposure allowed for the identification of genes responding specifically to induced, oxidative DNA damage. We also found that the presence of DNA damage alone was sufficient to cause an increase in intracellular ROS levels. These results, linking DNA damage and intracellular ROS production, may provide insight into the role of DNA damage in tumor progression and aging. To our knowledge, this is the first report establishing a relationship between H2O2-induced biological endpoints and specific oxidative DNA damage levels present in the genome.


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