Autophagy in Stem Cell Biology: A Perspective on Stem Cell Self-Renewal and Differentiation

Figure 1

Schematic depiction of the autophagy pathway and potential targets for modulating autophagy. mTORC1 activity suppression or AMPK activation leads to the activation of the ULK1 complex, formed by ULK1, ATG13, FIP200, and ATG101. The active ULK1 complex and the class III phosphatidylinositol-3-phosphate (PtdIns3P) kinase complex, formed by BECN1, ATG14, VPS15, VPS34, and Ambra1, control the initiation of autophagosome, via PtdIns3P formation and WIPI recruitment. The Atg-Atg12-Atg16 complex and LC3-II control the formation of autophagosome. Autophagy can be activated by drugs such as rapamycin that induce autophagy through mTOR inhibition. In contrast, inhibition of class III PI3K by 3-MA can inhibit autophagy. In addition, chloroquine inhibits lysosomal enzymes and also prevents the fusion of autophagosome and lysosome, resulting in the inhibition of autophagy.