Abstract
N-Acetyltransferase Mpr1 of Saccharomyces cerevisiae can reduce intracellular oxidation levels and protect yeast cells under oxidative stress, including H2O2, heat-shock, or freeze-thaw treatment. Unlike many antioxidant enzyme genes induced in response to oxidative stress, the MPR1 gene seems to be constitutively expressed in yeast cells. Based on a recent report that ethanol toxicity is correlated with the production of reactive oxygen species (ROS), we examined here the role of Mpr1 under ethanol stress conditions. The null mutant of the MPR1 and MPR2 genes showed hypersensitivity to ethanol stress, and the expression of the MPR1 gene conferred stress tolerance. We also found that yeast cells exhibited increased ROS levels during exposure to ethanol stress, and that Mpr1 protects yeast cells from ethanol stress by reducing intracellular ROS levels. When the MPR1 gene was overexpressed in antioxidant enzyme-deficient mutants, increased resistance to H2O2 or heat shock was observed in cells lacking the CTA1, CTT1, or GPX1 gene encoding catalase A, catalase T, or glutathione peroxidase, respectively. These results suggest that Mpr1 might compensate the function of enzymes that detoxify H2O2. Hence, Mpr1 has promising potential for the breeding of novel ethanol-tolerant yeast strains.
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Acknowledgment
We wish to thank M. Shichiri and M. Nomura (Fukui Prefectural University, Fukui, Japan) for assistance in the Northern analysis and H. Shimoi (National Research Institute of Brewing, Higashihiroshima, Japan) for the discussion on this work. We also thank G. Fink and C. Kaiser (Massachusetts Institute of Technology, Cambridge, MA) for providing yeast strains L5685 and CKY263, respectively. This work was supported by a grant for the Program for Promotion of Basic Research Activities for Innovative Biosciences (PROBRAIN) and by a grant-in-aid for the Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan (18380062) to H.T.
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Du, X., Takagi, H. N-Acetyltransferase Mpr1 confers ethanol tolerance on Saccharomyces cerevisiae by reducing reactive oxygen species. Appl Microbiol Biotechnol 75, 1343–1351 (2007). https://doi.org/10.1007/s00253-007-0940-x
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DOI: https://doi.org/10.1007/s00253-007-0940-x