Mitochondria Autophagy in Yeast

Department of Clinical Chemistry and Laboratory Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
Antioxidants & Redox Signaling (Impact Factor: 7.41). 05/2011; 14(10):1989-2001. DOI: 10.1089/ars.2010.3762
Source: PubMed


The mitochondrion is an organelle that carries out a number of important metabolic processes such as fatty acid oxidation, the citric acid cycle, and oxidative phosphorylation. However, this multitasking organelle also generates reactive oxygen species (ROS), which can cause oxidative stress resulting in self-damage. This type of mitochondrial damage can lead to the further production of ROS and a resulting downward spiral with regard to mitochondrial capability. This is extremely problematic because the accumulation of dysfunctional mitochondria is related to aging, cancer, and neurodegenerative diseases. Accordingly, appropriate quality control of this organelle is important to maintain proper cellular homeostasis. It has been thought that selective mitochondria autophagy (mitophagy) contributes to the maintenance of mitochondrial quality by eliminating damaged or excess mitochondria, although little is known about the mechanism. Recent studies in yeast identified several mitophagy-related proteins, which have been characterized with regard to their function and regulation. In this article, we review recent advances in the physiology and molecular mechanism of mitophagy and discuss the similarities and differences of this degradation process between yeast and mammalian cells.

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    • "Another group of upregulated genes was those related to autophagy. To date, more than 30 autophagy-related (ATG) genes have been identified for Saccharomyces cerevisiae and other fungi [34,35]. BLASTP search of the predicted T. reesei proteins ( "
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    • "Fluorescence microscopy of wild type and Δatg1 and Δatg8 reporter strains with GFP-labeled mitochondria revealed that degradation of the mitochondria in response to carbon starvation is impaired in autophagy-deficient mutants. In yeast, the degradation of excess mitochondria during the stationary phase constitutes a physiological adaptation to the reduced energy requirement of the cells (Kanki et al. 2011). Impairment of autophagy has been shown to lead to mitochondria dysfunction and the accumulation of ROS in yeast stationary phase cultures starved for nitrogen (Suzuki et al. 2011). "
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    • "Several lines of evidence suggest that the primary mechanism to eliminate dysfunctional, aged or excess mitochondria , promoting cell survival, is the selective form of autophagy, termed mitophagy [20] [21]. It has also been shown that the mitochondrial stress responses (MSRs) are mediated through the activity of the transcriptional coactivator peroxisome-proliferator-activated receptor coactivator-1 (PGC-1)α [22]. "
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