Macroautophagy/autophagy, a process that is highly conserved from yeast to mammals, delivers unwanted cellular contents to lysosomes or the vacuole for degradation. It has been reported that autophagy is crucial for maintaining glucose homeostasis. However, the mechanism by which energy deprivation induces autophagy is not well established. Recently, we found that Mec1/ATR, originally identified as a sensor of DNA damage, is essential for glucose starvation-induced autophagy. Mec1 is recruited to mitochondria where it is phosphorylated by activated Snf1 in response to glucose starvation. Phosphorylation of Mec1 leads to the assembly of a Snf1-Mec1-Atg1 module on mitochondria, which promotes the association of Atg1 with Atg13. Furthermore, we found that mitochondrial respiration is specifically required for glucose starvation-induced autophagy but not autophagy induced by canonical stimuli. The Snf1-Mec1-Atg1 module is essential for maintaining mitochondrial respiration and regulating glucose starvation-induced autophagy.
Keywords: Snf1-Mec1-Atg1; autophagy; energy deprivation; mitochondria; respiration.