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Figure. From: Staying alive.

FigureĀ 2. Autophagy is activated by low mTOR signaling and activation of ULK1. In starvation conditions, high TSC activity represses mTOR, which allows ULK1 to become active. After recruiting additional proteins to form a complex, ULK1 promotes autophagosome formation and autophagy. In contrast, high mTOR activity in high-nutrient conditions phorphorylates ULK1 and suppresses the induction of autophagy.

James R. Valcourt, et al. Cell Cycle. 2012 May 1;11(9):1680-1696.

Figure. From: Staying alive.

FigureĀ 1. External factors induce cell growth and suppress autophagy via Akt and TOR. Upon stimulation by external factors, such as growth factors, the receptor tyrosine kinase is phosphorylated and recruits PI3K. PI3K phosphorylates PtdIns(4,5)P2 to PtdIns(3,4,5)P3, which then recruits PDK and Akt to the cell membrane. Akt, when phosphorylated by mTORC2 and PDK, inhibits TSC, which in turn inhibits Rheb. When activated, Rheb promotes mTORC1 action, which leads to an increase in biosynthesis and suppression of autophagy via ULK1. Thus, nutrient-rich conditions lead to high activity of PI3K, Akt, and mTORC1, while nutrient depletion causes reduced PI3K activity and a resulting decrease in mTORC1 activity.

James R. Valcourt, et al. Cell Cycle. 2012 May 1;11(9):1680-1696.

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