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. Author manuscript; available in PMC: 2016 Mar 15.
Published in final edited form as: Front Biol (Beijing). 2015 Mar 30;10(2):154–164. doi: 10.1007/s11515-015-1354-2

Figure 2.

Figure 2

Regulation of autophagosome formation. Under nutrient-rich conditions, active mTORC1 inhibits the ULK1 kinase complex; whereas starvation activates AMPK, suppresses mTORC1 and induces ULK1, which upregulates another kinase complex, the PtdIns3K complex. Recruitment of Beclin 1 to the PtdIns3K complex is essential for the kinase activity, and is negatively regulated by sequestration of Beclin 1 by Bcl-2 and positively regulated by release of Beclin 1 upon JNK-mediated phosphorylation of Bcl-2. The PtdIns3K complex generates PI3P, which recruits additional PI3P-binding proteins (including WIPI and DFCP1) to promote autophagosome formation. Elongation of autophagosome membrane requires two ubiquitin-like conjugation systems, Atg12-Atg5-Atg16 and LC3-PE; the former acts as an E3 ligase to assist the conjugation of LC3 to PE. All the above molecules and pathways cooperate on the induction and formation of autophagosomes under stress conditions.