Insights into the relationship between the proteasome and autophagy in human and yeast cells |
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| Affiliation: | 1. CNRS, IBGC, UMR5095, 1 rue Camille Saint-Saëns, F-33000 Bordeaux, France;2. Université de Bordeaux, IBGC, UMR5095, 1 rue Camille Saint-Saëns, F-33000 Bordeaux, France;3. Comenius University, Faculty of Natural Sciences, Department of Biochemistry, Mlynská dolina CH1 84215, Bratislava, Slovak Republic;1. Gansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, School of Life Sciences, Lanzhou University, Lanzhou 730000, China;2. Gansu Provincial Hospital, Lanzhou 730030, China;1. Department of Toxicology, School of Public Health (Guangdong Provincial Key Laboratory of Tropical Disease Research), Southern Medical University, Guangzhou, 510515, China;2. Guangdong Laboratory Animals Monitoring Institute (Guangdong Provincial Key Laboratory of Laboratory Animals), Guangzhou, 510663, China;3. Bioland Laboratory (Guangzhou Regenerative Medicine and Health Guangdong Laboratory), Guangzhou, 510005, China;4. Department of Cardiology (Guangdong Provincial Key Laboratory of Shock and Microcirculation), Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China;1. Department of Biochemistry & Nutrition, Des Moines University, Des Moines, IA 50312, USA;2. Department of Microbiology & Immunology, Des Moines University, Des Moines, IA 50312, USA |
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| Abstract: | In eukaryotes, the ubiquitin-proteasome system (UPS) and autophagy are two major intracellular protein degradation pathways. Several lines of evidence support the emerging concept of a coordinated and complementary relationship between these two processes, and a particularly interesting finding is that the inhibition of the proteasome induces autophagy. Yet, there is limited knowledge of the regulation of the UPS by autophagy. In this study, we show that the disruption of ATG5 and ATG32 genes in yeast cells under both nutrient-deficient conditions as well as stress that causes mitochondrial dysfunction leads to an activation of proteasome. The same scenario occurs after pharmacological inhibition of basal autophagy in cultured human cells. Our findings underline the view that the two processes are interconnected and tend to compensate, to some extent, for each other's functions. |
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| Keywords: | Proteasome Autophagy Mitophagy Yeast Human cell lines |
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