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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    ABSTRACT: Renewable lignocellulosic biomass is an advantageous resource for the production of second generation biofuels and other biorefinery products. In Middle Europe, wheat straw is one of the most abundant low-cost sources of lignocellulosic biomass. For its efficient use, an efficient mix of cellulases and hemicellulases is required. In this paper, we investigated how cellulase production by T. reesei on wheat straw compares to that on lactose, the only soluble and also cheap inducing carbon source for enzyme production. We have examined and compared the transcriptome of T. reesei growing on wheat straw and lactose as carbon sources under otherwise similar conditions. Gene expression on wheat straw exceeded that on lactose, and 1619 genes were found to be only induced on wheat straw but not on lactose. They comprised 30% of the CAZome, but were also enriched in genes associated with phospholipid metabolism, DNA synthesis and repair, iron homeostatis and autophagy. Two thirds of the CAZome was expressed both on wheat straw as well as on lactose, but 60% of it at least >2-fold higher on the former. Major wheat straw specific genes comprised xylanases, chitinases and mannosidases. Interestingly, the latter two CAZyme families were significantly higher expressed in a strain in which xyr1 encoding the major regulator of cellulase and hemicellulase biosynthesis is non-functional. Our data reveal several major differences in the transcriptome between wheat straw and lactose which may be related to the higher enzyme formation on the former and their further investigation could lead to the development of methods for increasing enzyme production on lactose.
    Biotechnology for Biofuels 09/2013; 6(1):127. DOI:10.1186/1754-6834-6-127 · 6.04 Impact Factor
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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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    ABSTRACT: Autophagy is a well-conserved catabolic process constitutively active in eukaryotes that is involved in maintaining cellular homeostasis by the targeting of cytoplasmic content and organelles to vacuoles. Autophagy is strongly induced by the limitation of nutrients including carbon, nitrogen, and oxygen and is clearly associated with cell death. It has been demonstrated that the accumulation of empty hyphal compartments and cryptic growth in carbon-starved submerged cultures of the filamentous fungus Aspergillus niger is accompanied by a joint transcriptional induction of autophagy genes. This study examines the role of autophagy by deleting the atg1, atg8, and atg17 orthologs in A. niger and phenotypically analyzing the deletion mutants in surface and submerged cultures. The results indicate that atg1 and atg8 are essential for efficient autophagy, whereas deletion of atg17 has little to no effect on autophagy in A. niger. Depending on the kind of oxidative stress confronted with, autophagy deficiency renders A. niger either more resistant (menadione) or more sensitive (H2O2) to oxidative stress. Fluorescence microscopy showed that mitochondrial turnover upon carbon depletion in submerged cultures is severely blocked in autophagy-impaired A. niger mutants. Furthermore, automated image analysis demonstrated that autophagy promotes survival in maintained carbon-starved cultures of A. niger. Taken together, the results suggest that besides its function in nutrient recycling, autophagy plays important roles in physiological adaptation by organelle turnover and protection against cell death upon carbon depletion in submerged cultures.
    Applied Microbiology and Biotechnology 05/2013; 97(18). DOI:10.1007/s00253-013-4971-1 · 3.34 Impact Factor
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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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    ABSTRACT: Cell homeostasis results from the balance between cell capability to adapt or succumb to environmental stress. Mitochondria, in addition to supplying cellular energy, are involved in a range of processes deciding about cellular life or death. The crucial role of mitochondria in cell death is well recognized. Mitochondrial dysfunction has been associated with the death process and the onset of numerous diseases. Yet, mitochondrial involvement in cellular adaptation to stress is still largely unexplored. Strong interest exists in pharmacological manipulation of mitochondrial metabolism and signaling. The yeast Saccharomyces cerevisiae has proven a valuable model organism in which several intracellular processes have been characterized in great detail, including the retrograde response to mitochondrial dysfunction and, more recently, programmed cell death. In this paper we review experimental evidences of mitochondrial involvement in cytoprotection and propose yeast as a model system to investigate the role of mitochondria in the cross-talk between prosurvival and prodeath pathways.
    The Scientific World Journal 02/2012; 2012:912147. DOI:10.1100/2012/912147 · 1.73 Impact Factor
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