Publication: Vacuolar H<sup>+</sup>-ATPase protects Saccharomyces cerevisiae cells against ethanolinduced oxidative and cell wall stresses
Issued Date
2016-05-01
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ISSN
10985336
00992240
00992240
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2-s2.0-84966573867
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Mahidol University
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SCOPUS
Bibliographic Citation
Applied and Environmental Microbiology. Vol.82, No.10 (2016), 3121-3130
Suggested Citation
Sirikarn Charoenbhakdi, Thanittra Dokpikul, Thanawat Burphan, Todsapol Techo, Choowong Auesukaree Vacuolar H<sup>+</sup>-ATPase protects Saccharomyces cerevisiae cells against ethanolinduced oxidative and cell wall stresses. Applied and Environmental Microbiology. Vol.82, No.10 (2016), 3121-3130. doi:10.1128/AEM.00376-16 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/40959
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Title
Vacuolar H<sup>+</sup>-ATPase protects Saccharomyces cerevisiae cells against ethanolinduced oxidative and cell wall stresses
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Abstract
© 2016, American Society for Microbiology. During fermentation, increased ethanol concentration is a major stress for yeast cells. Vacuolar H+-ATPase (V-ATPase), which plays an important role in the maintenance of intracellular pH homeostasis through vacuolar acidification, has been shown to be required for tolerance to straight-chain alcohols, including ethanol. Since ethanol is known to increase membrane permeability to protons, which then promotes intracellular acidification, it is possible that the V-ATPase is required for recovery from alcohol-induced intracellular acidification. In this study, we show that the effects of straight-chain alcohols on membrane permeabilization and acidification of the cytosol and vacuole are strongly dependent on their lipophilicity. These findings suggest that the membrane-permeabilizing effect of straight-chain alcohols induces cytosolic and vacuolar acidification in a lipophilicity-dependent manner. Surprisingly, after ethanol challenge, the cytosolic pH in Δvma2 and Δvma3 mutants lacking V-ATPase activity was similar to that of the wild-type strain. It is therefore unlikely that the ethanol-sensitive phenotype of vma mutants resulted from severe cytosolic acidification. Interestingly, the vma mutants exposed to ethanol exhibited a delay in cell wall remodeling and a significant increase in intracellular reactive oxygen species (ROS). These findings suggest a role for V-ATPase in the regulation of the cell wall stress response and the prevention of endogenous oxidative stress in response to ethanol.