2011 February ; 13(2): 132–141. doi:10.1038/ncb2152 | Joungmok Kim, Mondira Kundu, Benoit Viollet, and Kun-Liang Guan
Autophagy is a cellular process that degrades components to maintain viability under nutrient limitation. AMPK and mTOR, key energy sensors, regulate autophagy. AMPK promotes autophagy by activating Ulk1 through phosphorylation at Ser 317 and Ser 777 under glucose starvation. mTOR inhibits autophagy by phosphorylating Ulk1 at Ser 757, disrupting its interaction with AMPK. This coordinated phosphorylation is crucial for autophagy induction. The study reveals a signaling mechanism for Ulk1 regulation and autophagy induction in response to nutrient signaling.Autophagy is a cellular process that degrades components to maintain viability under nutrient limitation. AMPK and mTOR, key energy sensors, regulate autophagy. AMPK promotes autophagy by activating Ulk1 through phosphorylation at Ser 317 and Ser 777 under glucose starvation. mTOR inhibits autophagy by phosphorylating Ulk1 at Ser 757, disrupting its interaction with AMPK. This coordinated phosphorylation is crucial for autophagy induction. The study reveals a signaling mechanism for Ulk1 regulation and autophagy induction in response to nutrient signaling.