Abstract
Autophagy, a process by which cells degrade their own components within lysosomes, is a major homeostatic mechanism that favors adaptation and survival under nutrient-deficient conditions. Starvation increases the number and size of autophagosomes in many tissues, suggesting that autophagy is a critical component of the body's response to nutrient deprivation and amino acid/fuel homeostasis. In addition, autophagy has been shown to play a critical role in maintaining amino acid and energy homeostasis in neonates during the transitional hours immediately following birth. The recent identification of functional mammalian orthologues of Atg14 and Atg17 has completed the identification of mammalian orthologues of all of the core yeast autophagy genes. In addition, the recent placement of the Atg1*Atg13*Atg17 complex downstream of mTORC1 has provided at least one pathway by which changes in nutrient availability regulate autophagy.
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