Journal
AUTOPHAGY
Volume 16, Issue 6, Pages 1154-1156Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2020.1749368
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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Funding
- German Research Foundation (DFG) [SFB746, SFB850, 7 SFB1381]
- Germany's Excellence Strategy [CIBSS - EXC-2189, 8 390939984]
- German Excellence Initiative [BIOSS - EXC 294]
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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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