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BioMed Research International
Volume 2017, Article ID 7587395, 8 pages
Research Article

MET18 Deficiency Increases the Sensitivity of Yeast to Oxidative Stress and Shortens Replicative Lifespan by Inhibiting Catalase Activity

1Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Chongqing Medical University, No. 1 Yixueyuan Road, Yuzhong District, Chongqing 400016, China
2Institute of Aging Research, Guangdong Medical University, Dongguan 523808, China
3Key Laboratory for Medical Molecular Diagnostics of Guangdong Province, Dongguan 523808, China
4School of Laboratory Medicine, Guangdong Medical University, Dongguan 523808, China

Correspondence should be addressed to Zhiguang Tu; moc.anis@gdgnaugihzut

Received 12 April 2017; Accepted 20 June 2017; Published 30 July 2017

Academic Editor: Paul W. Doetsch

Copyright © 2017 Ya-qin Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Yeast MET18, a subunit of the cytosolic iron-sulfur (Fe/S) protein assembly (CIA) machinery which is responsible for the maturation of Fe/S proteins, has been reported to participate in the oxidative stress response. However, the underlying molecular mechanisms remain unclear. In this study, we constructed a MET18/met18Δ heterozygous mutant yeast strain and found that MET18 deficiency in yeast cells impaired oxidative stress resistance as evidenced by increased sensitivity to hydrogen peroxide (H2O2) and cumene hydroperoxide (CHP). Mechanistically, the mRNA levels of catalase A (CTA1) and catalase T (CTT1) as well as the total catalase activity were significantly reduced in MET18-deficient cells. In contrast, overexpression of CTT1 or CTA1 in MET18-deficient cells significantly increased the intracellular catalase activity and enhanced the resistance ability against H2O2 and CHP. In addition, MET18 deficiency diminished the replicative capacity of yeast cells as evidenced by the shortened replicative lifespan, which can be restored by CTT1 overexpression, but not by CTA1, in the MET18-deficient cells. These results suggest that MET18, in a catalase-dependent manner, plays an essential role in enhancing the resistance of yeast cells to oxidative stress and increasing the replicative capacity of yeast cells.