Document Detail

Mitophagy plays an essential role in reducing mitochondrial production of reactive oxygen species and mutation of mitochondrial DNA by maintaining mitochondrial quantity and quality in yeast.
MedLine Citation:
PMID:  22157017     Owner:  NLM     Status:  MEDLINE    
In mammalian cells, the autophagy-dependent degradation of mitochondria (mitophagy) is thought to maintain mitochondrial quality by eliminating damaged mitochondria. However, the physiological importance of mitophagy has not been clarified in yeast. Here, we investigated the physiological role of mitophagy in yeast using mitophagy-deficient atg32- or atg11-knock-out cells. When wild-type yeast cells in respiratory growth encounter nitrogen starvation, mitophagy is initiated, excess mitochondria are degraded, and reactive oxygen species (ROS) production from mitochondria is suppressed; as a result, the mitochondria escape oxidative damage. On the other hand, in nitrogen-starved mitophagy-deficient yeast, excess mitochondria are not degraded and the undegraded mitochondria spontaneously age and produce surplus ROS. The surplus ROS damage the mitochondria themselves and the damaged mitochondria produce more ROS in a vicious circle, ultimately leading to mitochondrial DNA deletion and the so-called "petite-mutant" phenotype. Cells strictly regulate mitochondrial quantity and quality because mitochondria produce both necessary energy and harmful ROS. Mitophagy contributes to this process by eliminating the mitochondria to a basal level to fulfill cellular energy requirements and preventing excess ROS production.
Yusuke Kurihara; Tomotake Kanki; Yoshimasa Aoki; Yuko Hirota; Tetsu Saigusa; Takeshi Uchiumi; Dongchon Kang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-12-07
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  287     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2012-01-30     Completed Date:  2012-03-22     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3265-72     Citation Subset:  IM    
Department of Clinical Chemistry and Laboratory Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka 812-8582, Japan.
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MeSH Terms
DNA, Fungal / genetics,  metabolism*
DNA, Mitochondrial / genetics,  metabolism*
Energy Metabolism / physiology*
Mitochondria / genetics,  metabolism*
Reactive Oxygen Species / metabolism*
Receptors, Cytoplasmic and Nuclear / genetics,  metabolism
Saccharomyces cerevisiae / genetics,  metabolism*
Saccharomyces cerevisiae Proteins / genetics,  metabolism
Vesicular Transport Proteins / genetics,  metabolism
Reg. No./Substance:
0/Atg11 protein, S cerevisiae; 0/Atg32 protein, S cerevisiae; 0/DNA, Fungal; 0/DNA, Mitochondrial; 0/Reactive Oxygen Species; 0/Receptors, Cytoplasmic and Nuclear; 0/Saccharomyces cerevisiae Proteins; 0/Vesicular Transport Proteins

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