Formation of a Snf1-Mec1-Atg1 Module on Mitochondria Governs Energy Deprivation-Induced Autophagy by Regulating Mitochondrial Respiration

Publication date: 10 April 2017
Source:Developmental Cell, Volume 41, Issue 1
Author(s): Cong Yi, Jingjing Tong, Puzhong Lu, Yizheng Wang, Jinxie Zhang, Chen Sun, Kangning Yuan, Renyu Xue, Bing Zou, Nianzhong Li, Shuhua Xiao, Chong Dai, Yuwei Huang, Liling Xu, Lin Li, She Chen, Di Miao, Haiteng Deng, Hongliang Li, Li Yu
Autophagy is essential for maintaining glucose homeostasis, but the mechanism by which energy deprivation activates autophagy is not fully understood. We show that Mec1/ATR, a member of the DNA damage response pathway, is essential for glucose starvation-induced autophagy. Mec1, Atg13, Atg1, and the energy-sensing kinase Snf1 are recruited to mitochondria shortly after glucose starvation. Mec1 is recruited through the adaptor protein Ggc1. Snf1 phosphorylates Mec1 on the mitochondrial surface, leading to recruitment of Atg1 to mitochondria. Furthermore, the Snf1-mediated Mec1 phosphorylation and mitochondrial recruitment of Atg1 are essential for maintaining mitochondrial respiration during glucose starvation, and active mitochondrial respiration is required for energy deprivation-activated autophagy. Thus, formation of a Snf1-Mec1-Atg1 module on mitochondria governs energy deprivation-induced autophagy by regulating mitochondrial respiration.

Graphical abstract

Teaser

Yi, Tong et al. study the mechanisms underlying induction of autophagy during energy deprivation. They show that Mec1/ATR, a component of the DNA damage response pathway, is essential for glucose starvation-induced autophagy and that a Snf1-Mec1-Atg1 module on the surface of mitochondria governs energy deprivation-induced autophagy by regulating mitochondrial respiration.


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