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. Author manuscript; available in PMC: 2019 Feb 1.
Published in final edited form as: Curr Opin Immunol. 2017 Nov 7;50:21–31. doi: 10.1016/j.coi.2017.10.004

Figure 1. The molecular mechanisms of canonical autophagy.

Figure 1

Normally held in check by mTOR, autophagy-inducing signals (such as nutrient deprivation) triggers the activation of AMPK, whose kinase activity simultaneously inhibits mTOR and activates the pre-initiation complex (ULK1/2, ATG13, FIP200). This complex then activates the Class III PI3K complex, composed of VPS34 and Beclin 1, along with either ATG14 or UVRAG. The Class III PI3K complex produces phosphatidylinositol 3-phosphate (PI3P), which acts as recruitment signal for the downstream ubiquitin-like conjugation systems, the ATG12-5 system and the LC3-PE system. The activity and coordination of these two systems facilitates the curvature and sealing of the autophagosome, as well as the lipidation and embedding of LC3-PE into the autophagosomal membrane.