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Vacuolar H + ‐ ATPase is involved in preventing heavy metal‐induced oxidative stress in Saccharomyces cerevisiae
Author(s) -
Techo Todsapol,
Jindarungrueng Supat,
Tatip Supinda,
Limcharoensuk Tossapol,
Pokethitiyook Prayad,
Kruatrachue Maleeya,
Auesukaree Choowong
Publication year - 2020
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/1462-2920.15022
Subject(s) - biology , cytosol , vacuole , reactive oxygen species , biochemistry , atpase , oxidative stress , saccharomyces cerevisiae , intracellular , microbiology and biotechnology , superoxide dismutase , yeast , enzyme , cytoplasm
Summary In Saccharomyces cerevisiae , vacuolar H + ‐ATPase (V‐ATPase) involved in the regulation of intracellular pH homeostasis has been shown to be important for tolerances to cadmium, cobalt and nickel. However, the molecular mechanism underlying the protective role of V‐ATPase against these metals remains unclear. In this study, we show that cadmium, cobalt and nickel disturbed intracellular pH balance by triggering cytosolic acidification and vacuolar alkalinization, likely via their membrane permeabilizing effects. Since V‐ATPase plays a crucial role in pumping excessive cytosolic protons into the vacuole, the metal‐sensitive phenotypes of the Δvma2 and Δvma3 mutants lacking V‐ATPase activity were supposed to result from highly acidified cytosol. However, we found that the metal‐sensitive phenotypes of these mutants were caused by increased production of reactive oxygen species, likely as a result of decreased expression and activities of manganese superoxide dismutase and catalase. In addition, the loss of V‐ATPase function led to aberrant vacuolar morphology and defective endocytic trafficking. Furthermore, the sensitivities of the Δvma mutants to other chemical compounds (i.e. acetic acid, H 2 O 2 , menadione, tunicamycin and cycloheximide) were a consequence of increased endogenous oxidative stress. These findings, therefore, suggest the important role of V‐ATPase in preventing endogenous oxidative stress induced by metals and other chemical compounds.