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PMID: 15603750 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S. Review

Yeast signaling pathways in the oxidative stress response.

Mutation research ·Vol. 569 ·No. 1-2 ·2005-01-06 ·Pages 13-27

Ikner A, Shiozaki K

Abstract

Oxidative stress that generates the reactive oxygen species (ROS) is one of the major causes of DNA damage and mutations. The "DNA damage checkpoint" that arrests cell cycle and repairs damaged DNA has been a focus of recent studies, and the genetically amenable model systems provided by yeasts have been playing a leading role in the eukaryotic checkpoint research. However, means to eliminate ROS are likely to be as important as the DNA repair mechanisms in order to suppress mutations in the chromosomal DNA, and yeasts also serve as excellent models to understand how eukaryotes combat oxidative stress. In this article, we present an overview of the signaling pathways that sense oxidative stress and induce expression of various anti-oxidant genes in the budding yeast Saccharomyces cerevisiae, the fission yeast Schizosaccharomyces pombe and the pathogenic yeast Candida albicans. Three conserved signaling modules have been identified in the oxidative stress response of these diverse yeast species: the stress-responsive MAP kinase cascade, the multistep phosphorelay and the AP-1-like transcription factor. The structure and function of these signaling modules are discussed.

MeSH Terms
Mitogen-Activated Protein Kinases/genetics,metabolism Oxidative Stress/genetics Phosphorylation Reactive Oxygen Species/metabolism Signal Transduction/genetics Transcription Factor AP-1/genetics,metabolism Transcriptional Activation Yeasts/enzymology,genetics,metabolism
Chemicals
Reactive Oxygen Species Transcription Factor AP-1 Mitogen-Activated Protein Kinases
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Ikner Aminah
Section of Microbiology, Division of Biological Sciences, University of California, Davis, CA 95616, USA.
Shiozaki Kazuhiro
Article Info
Journal
Mutation research
Abbr.
Mutat Res
ISSN
0027-5107
Published
2005-01-06
Pages
13-27
Language
English
Region
Netherlands
NLM ID
0400763
Subset
IM
Grants
NIGMS NIH HHS · GM059788 · United States
NIGMS NIH HHS · GM070405 · United States
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