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. Author manuscript; available in PMC: 2017 Aug 28.
Published in final edited form as: J Mol Biol. 2016 Jul 22;428(17):3387–3398. doi: 10.1016/j.jmb.2016.07.007

Figure 1. Sequential steps of canonical autophagy.

Figure 1

In the presence of amino acids, growth factors and energy, the mTOR complex represses autophagy by inhibiting the kinase activity of ULK1. The PI3K/Akt pathway inhibits autophagy, while AMPK activates autophagy by controlling mTOR activation under nutrient-limiting conditions. Upon autophagy induction (1), the ULK1 complex activates the BECN1/VPS34 complex to initiate (2) phagophore formation and nucleation. BECN1 can be activated directly by the IRE1α/JNK pathway or inhibited by the pharmacological drug 3-methyladenine (3-MA). Phagophore elongation (3) proceeds to engulf and sequester autophagic cargo and the phagophore membrane acquires LC3. Ubiquitin-like conjugation systems mediate the closure of the autophagosome (4). Maturation of the autophagosome (5) occurs via fusion with late endocytic/lysosomal compartments, forming the autolysosome where material is degraded. Autolysosomes are then recycled in a process that allows for lysosome reformation (6).