A biological network in Saccharomyces cerevisiae prevents the deleterious effects of endogenous oxidative DNA damage.

In this study, we used Saccharomyces cerevisiae to identify a biological network that prevents the deleterious effects of endogenous reactive oxygen species. The absence of Tsa1, a key peroxiredoxin, caused increased rates of mutations, chromosomal rearrangements, and recombination. Defects in recombinational DNA double strand break repair, Rad6-mediated postreplicative repair, and ...
DNA damage and replication checkpoints caused growth defects or lethality in the absence of Tsa1. In addition, the mutator phenotypes caused by a tsa1 mutation were significantly aggravated by defects in Ogg1, mismatch repair, or checkpoints. These results indicate that increased endogenous oxidative stress has broad effects on genome stability and is highly sensitive to the functional state of DNA repair and checkpoints. These findings may provide insight in understanding the consequences of various pathophysiological processes in regard to genomic instability.
Mesh Terms:
DNA Damage, DNA Glycosylases, DNA Repair, DNA Replication, Genetic Complementation Test, Genome, Fungal, Genotype, Models, Genetic, Mutation, Oxidative Stress, Peroxidases, Phenotype, Reactive Oxygen Species, Recombination, Genetic, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Telomere, Ubiquitin-Conjugating Enzymes
Mol. Cell
Date: Mar. 04, 2005
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