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Loss of Cytochrome c Oxidase Promotes RAS-Dependent ROS Production from the ER Resident NADPH Oxidase, Yno1p, in Yeast.

Leadsham, Jane E., Sanders, Geraldine, Giannaki, Samantha, Bastow, Emma L., Hutton, Rachael, Naemi, Wesley R., Breitenbach, Michael, Gourlay, Campbell W. (2013) Loss of Cytochrome c Oxidase Promotes RAS-Dependent ROS Production from the ER Resident NADPH Oxidase, Yno1p, in Yeast. Cell Metabolism, 18 (2). pp. 279-286. ISSN 1932-7420. (doi:10.1016/j.cmet.2013.07.005) (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided)

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Official URL
http://dx.doi.org/10.1016/j.cmet.2013.07.005

Abstract

Many disease states, including the aging process, are associated with the accumulation of mitochondria harboring respiratory dysfunction. Mitochondrial dysfunction is often accompanied by increased ROS levels that can contribute to cellular dysfunction and disease etiology. Here we use the model eukaryote S. cerevisiae to investigate whether reduced cytochrome c oxidase (COX) activity, commonly reported in aging organisms and associated with neurodegenerative disorders, leads to ROS production from mitochondria. We provide evidence that although reduced COX complex activity correlates with ROS accumulation, mitochondria are not the major production center. Instead we show that COX-deficient mitochondria activate Ras upon their outer membrane that establishes a pro-ROS accumulation environment by suppressing antioxidant defenses and the ERAD-mediated turnover of the ER-localized NADPH oxidase Yno1p. Our data suggest that dysfunctional mitochondria can serve as a signaling platform to promote the loss of redox homeostasis, ROS accumulation, and accelerate aging in yeast.

Item Type: Article
DOI/Identification number: 10.1016/j.cmet.2013.07.005
Subjects: Q Science
Q Science > Q Science (General)
Divisions: Faculties > Sciences > School of Biosciences
Depositing User: Campbell Gourlay
Date Deposited: 28 Aug 2013 08:49 UTC
Last Modified: 06 Feb 2020 04:07 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/35035 (The current URI for this page, for reference purposes)
Gourlay, Campbell W.: https://orcid.org/0000-0002-2373-6788
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