Hyperoxidation of mitochondrial peroxiredoxin limits H2 O2 -induced cell death in yeast.
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ABSTRACT: Hydrogen peroxide (H2 O2 ) plays important roles in cellular signaling, yet nonetheless is toxic at higher concentrations. Surprisingly, the mechanism(s) of cellular H2 O2 toxicity remain poorly understood. Here, we reveal an important role for mitochondrial 1-Cys peroxiredoxin from budding yeast, Prx1, in regulating H2 O2 -induced cell death. We show that Prx1 efficiently transfers oxidative equivalents from H2 O2 to the mitochondrial glutathione pool. Deletion of PRX1 abrogates glutathione oxidation and leads to a cytosolic adaptive response involving upregulation of the catalase, Ctt1. Both of these effects contribute to improved cell viability following an acute H2 O2 challenge
SUBMITTER: Calabrese G
PROVIDER: S-EPMC6745495 | biostudies-literature | 2019 Sep
REPOSITORIES: biostudies-literature
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