TORC2-SGK-1 signaling integrates external signals to regulate autophagic turnover of mitochondria via mtROS |
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Authors: | Thomas Heimbucher Wenjing Qi |
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Institution: | 1. Bioinformatics and Molecular Genetics, Faculty of Biology, University of Freiburg , Freiburg, Germany;2. Bioinformatics and Molecular Genetics, Faculty of Biology, University of Freiburg , Freiburg, Germany;3. Signalling Research Centres BIOSS and CIBSS, University of Freiburg , Freiburg, Germany https://orcid.org/0000-0002-9287-5837 |
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Abstract: | ABSTRACT Macroautophagy/autophagy is an evolutionarily conserved cellular degradation and recycling process that is tightly regulated by external stimuli, diet, and stress. Our recent findings suggest that in C. elegans, a nutrient sensing pathway mediated by MTORC2 (mechanistic target of rapamycin kinase complex 2) and its downstream effector kinase SGK-1 (serum- and glucocorticoid-inducible kinase homolog 1) suppresses autophagy, involving mitophagy. Induced autophagy/mitophagy in MTORC2-deficient animals slows down development and impairs reproduction independently of the SGK-1 effectors DAF-16/FOXO and SKN-1/NFE2L2/NRF2. In this punctum, we discuss how TORC2-SGK-1 signaling might regulate autophagic turnover and its impact on mitochondrial homeostasis via linking mitochondria-derived reactive oxygen species (mtROS) production to mitophagic turnover. |
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Keywords: | Autophagy mitophagy MTORC (mechanistic target of rapamycin kinase complex) ROS (reactive oxygen species) SGK-1 (serum- and glucocorticoid-inducible kinase homolog 1) VDAC1 (voltage dependent anion channel 1) |
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