MITOCHONDRIAL SUPEROXIDE-DISMUTASE IS ESSENTIAL FOR ETHANOL TOLERANCEOF SACCHAROMYCES-CEREVISIAE IN THE POST-DIAUXIC PHASE

Citation
V. Costa et al., MITOCHONDRIAL SUPEROXIDE-DISMUTASE IS ESSENTIAL FOR ETHANOL TOLERANCEOF SACCHAROMYCES-CEREVISIAE IN THE POST-DIAUXIC PHASE, Microbiology, 143, 1997, pp. 1649-1656
Citations number
39
Categorie Soggetti
Microbiology
Journal title
ISSN journal
13500872
Volume
143
Year of publication
1997
Part
5
Pages
1649 - 1656
Database
ISI
SICI code
1350-0872(1997)143:<1649:MSIEFE>2.0.ZU;2-P
Abstract
This work reports the role of both superoxide dismutases - CuZnSOD (en coded by SOD1) and MnSOD (encoded by SOD2)- in the build-up of toleran ce to ethanol during growth of Saccharomyces cerevisiae from exponenti al to post-diauxic phase. Both enzyme activities increase from the exp onential phase to the diauxic shift and from the diauxic shift to the post-diauxic phase. The levels of mRNA-SOD1 and mRNA-SOD2 increase fro m the exponential phase to the diauxic shift; however, during the post -diauxic phase mRNA-SOD1 levels decrease while mRNA-SOD2 levels remain unchanged. These data indicate the existence of two regulatory mechan isms involved in the induction of SOD activity during growth: synthesi s de novo of the proteins (until the diauxic shift), and post-transcri ptional or post-translational regulation (during the post-diauxic phas e). Ethanol does not alter the activities of either enzyme in cells fr om the diauxic shift or post-diauxic phases, although the respective m RNA levels decrease in post-diauxic-phase cells treated with ethanol ( 14% or 20%). Results of experiments with sod1 and sod2 mutants show th at MnSOD, but not CuZnSOD, is essential for ethanol tolerance of diaux ic-shift and post-diauxic-phase cells. Evidence that ethanol toxicity is correlated with the production of reactive oxygen species in the mi tochondria is obtained from results with respiration-deficient mutants . In these cells, the induction of superoxide dismutase activity by et hanol is low; also, the respiratory deficiency restores the capacity o f sod2 cells to aquire ethanol tolerance.