Bioinformatics and Molecular Genetics, Faculty of Biology, University of Freiburg , Freiburg, Germany.
Signalling Research Centres BIOSS and CIBSS, University of Freiburg , Freiburg, Germany.
Autophagy. 2020 Jun;16(6):1154-1156. doi: 10.1080/15548627.2020.1749368. Epub 2020 Apr 15.
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 , 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.
自噬是一种进化上保守的细胞降解和再循环过程，受到外部刺激、饮食和应激的严格调节。我们最近的研究结果表明，在 中，一种由 MTORC2（雷帕霉素靶蛋白激酶复合物 2）及其下游效应激酶 SGK-1（血清和糖皮质激素诱导的激酶同源物 1）介导的营养感应途径抑制自噬，涉及线粒体自噬。MTORC2 缺陷动物中诱导的自噬/线粒体自噬会减缓发育并损害繁殖，而与 SGK-1 效应物 DAF-16/FOXO 和 SKN-1/NFE2L2/NRF2 无关。在这一关键点上，我们讨论了 TORC2-SGK-1 信号如何通过将线粒体来源的活性氧（mtROS）产生与线粒体自噬周转联系起来，调节自噬周转及其对线粒体动态平衡的影响。
