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. 2019 Mar 4;218(3):757–770. doi: 10.1083/jcb.201810099

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© 2019 Zhao and Zhang

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 4. — Nutrient status regulates autophagosome maturation through multiple mechanisms. Starvation decreases O-GlcNAcylation of SNAP29 and promotes its interaction with STX17 and VAMP8 to form trans-SNARE complexes for autophagosome–LE/lysosome fusion. Starvation-induced de-O-GlcNAcylation of GRASP55 causes its translocation to autophagosomes. De-O-GlcNAcylated GRASP55 simultaneously binds to LC3 and LAMP2 to facilitate autophagosome maturation. Inhibition of mTORC1 activity by starvation leads to dephosphorylation of UVRAG, which releases Rubicon and subsequently recruits HOPS to promote autophagosome fusion. The transcription of a network of genes involved in autophagosome–lysosome fusion is activated by the transcription factor TFEB and inhibited by the transcriptional repressor ZKSCAN3. Starvation triggers dephosphorylation of TFEB, resulting in its nuclear translocation. The translocation of ZKSCAN3 out of the nucleus is also promoted by nutrient deficiency.