Publication: Vacuolar H<sup>+</sup>-ATPase is involved in preventing heavy metal-induced oxidative stress in Saccharomyces cerevisiae
Issued Date
2020-01-01
Resource Type
ISSN
14622920
14622912
14622912
Other identifier(s)
2-s2.0-85084239294
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Environmental Microbiology. (2020)
Suggested Citation
Todsapol Techo, Supat Jindarungrueng, Supinda Tatip, Tossapol Limcharoensuk, Prayad Pokethitiyook, Maleeya Kruatrachue, Choowong Auesukaree Vacuolar H<sup>+</sup>-ATPase is involved in preventing heavy metal-induced oxidative stress in Saccharomyces cerevisiae. Environmental Microbiology. (2020). doi:10.1111/1462-2920.15022 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/56093
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Vacuolar H<sup>+</sup>-ATPase is involved in preventing heavy metal-induced oxidative stress in Saccharomyces cerevisiae
Other Contributor(s)
Abstract
© 2020 Society for Applied Microbiology and John Wiley & Sons Ltd. 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, H2O2, 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.