11 research outputs found
Contribution of Yap 1 towards S. cervisiae adaptation to arsenic mediated oxidative stress
Post-PrintIn the budding yeast Saccharomyces cerevisiae arsenic detoxification involves the
activation Yap8, a member of the Yap family of transcription factors, which in turn
regulates ACR2 and ACR3, encoding an arsenate reductase and a plasma membrane
arsenite efflux-protein, respectively. In addition, Yap1 is involved in the arsenic
adaptation process through regulating the expression of the vacuolar-pump encoded by
YCF1 and also contributing to the regulation of ACR genes. Here we show that Yap1 is
also involved in the removal of ROS generated by arsenic compounds. Data on lipid
peroxidation and intracellular oxidation indicate that deletion of YAP1 and YAP8
triggers cellular oxidation mediated by inorganic arsenic. In spite of the increased
amounts of As(III) absorbed by the yap8 mutant, the enhanced transcriptional activation
of the antioxidant genes such as GSH1, SOD1 and TRX2 may prevent protein oxidation.
In contrast, the yap1 mutant exhibits high contents of protein carbonyl groups and the
GSSG:GSH ratio is severely disturbed upon exposure to arsenic compounds in these
cells. These results point to an additional level of Yap1 contribution to arsenic stress
responses by preventing oxidative damage in cells exposed to these compounds.
Transcriptional profiling revealed that genes of the functional categories related with
sulphur and methionine metabolism and with the maintenance of the cell redox
homeostasis are activated to mediate adaptation of the wild type strain to 2 mM arsenate
treatmen