Hyperosmotic stress triggers a great variety of adaptive responses in eukaryotic cells that affect many different physiological functions. Here we investigate the role of the mitochondria during osmostress adaptation in budding yeast. Mitochondrial function is generally required for proper salt and osmotic stress adaptation since mutants with defects in many different mitochondrial components show hypersensitivity to increased NaCl and KCl concentrations. Mitochondrial protein abundance rapidly increases upon osmoshock in a selective manner, as it affects Calvin cycle enzymes (Sdh2, Cit1) and components of the electron transport chain (Cox6), but not the ATP synthase complex (Atp5). Transcription of the SDH2, CIT1 and COX6 genes is several fold induced within the first minutes of osmotic shock, dependent to various degree on the Hog1 and Snf1 protein kinases. Mitochondrial succinate dehydrogenase enzyme activity is stimulated upon osmostress in a Snf1 dependent manner. The osmosensitivity of mitochondrial mutants is not caused by impaired stress-activated transcription or by a general depletion of the cellular ATP pool during osmostress. We finally show that the growth defect of mitochondrial mutants in high salt medium can be partially rescued by supplementation of glutathione. Additionally, mitochondrial defects cause the hyperaccumulation of reactive oxygen species during salt stress. Our results indicate that the antioxidant function of the mitochondria might play an important role in the adaptation to hyperosmotic stress.
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