TORC2-SGK-1 signaling integrates external signals to regulate autophagic turnover of mitochondria via mtROS.
Thomas HeimbucherWenjing QiRalf BaumeisterPublished in: Autophagy (2020)
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.
Keyphrases
- cell death
- reactive oxygen species
- oxidative stress
- signaling pathway
- bone mineral density
- protein kinase
- transcription factor
- endoplasmic reticulum stress
- diabetic rats
- tyrosine kinase
- physical activity
- postmenopausal women
- nlrp inflammasome
- type iii
- weight loss
- dendritic cells
- immune response
- body composition
- drug induced
- stress induced
- cell proliferation