Health & Environmental Research Online (HERO)


Print Feedback Export to File
516298 
Journal Article 
DNA damage-induced reactive oxygen species (ROS) stress response in Saccharomyces cerevisiae 
Rowe, LA; Degtyareva, N; Doetsch, PW 
2008 
Yes 
Free Radical Biology and Medicine
ISSN: 0891-5849
EISSN: 1873-4596 
45 
8 
1167-1177 
English 
Cells are exposed to both endogenous and exogenous sources of reactive oxygen species (ROS). At high levels, ROS can lead to impaired physiological function through cellular damage of DNA, proteins, lipids, and other macromolecules, which can lead to certain human pathologies including cancers, neurodegenerative disorders, and cardiovascular disease, as well as aging. We have employed Saccharomyces cerevisiae as a model system to examine the levels and types of ROS that are produced in response to DNA damage in isogenic strains with different DNA repair capacities. We find that when DNA damage is introduced into cells from exogenous or endogenous sources there is an increase in the amount of intracellular ROS which is not directly related to cell death. We have examined the spectrum of ROS in order to elucidate its role in the cellular response to DNA damage. As an independent verification of the DNA damage-induced ROS response, we show that a major activator of the oxidative stress response, Yap1, relocalizes to the nucleus following exposure to the DNA-alkylating agent methyl methanesulfonate. Our results indicate that the DNA damage-induced increase in intracellular ROS levels is a generalized stress response that is likely to function in various signaling pathways. (C) 2008 Elsevier Inc. All rights reserved. 
Reactive oxygen species; DNA damage; Genotoxic stress; DNA repair; Oxidative stress response; Yap1 transcription factor; nucleotide excision-repair; oxidative stress; transcription factor; free-radicals; dihydrorhodamine 123; activator proteins; endothelial-cells; hydrogen-peroxide; nuclear export; yeast