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Updated: Jan 11, 2026
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Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles
Published on: October 18, 2024
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mTORC1 regulates autophagosomal components recycling through SNX16 phosphorylation
Huilin Que1, Fengping Liu1, Yang Chen2,3
1Department of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Disease, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China.
Summary
SNX16 is identified as a key component of the recycler complex, essential for autophagosomal components recycling (ACR) during autophagy. This process is regulated by mTORC1, linking it to autophagic activity maintenance.
Area of Science:
- Cell Biology
- Molecular Biology
- Autophagy Research
Background:
- Autophagy degrades cellular waste, recycling components via autolysosomes.
- Autophagosomal components recycling (ACR) maintains autophagic activity but its mechanisms are unclear.
Purpose of the Study:
- To identify molecular machinery and upstream regulators of ACR.
- To elucidate the role of SNX16 in the ACR process.
Main Methods:
- Protein localization studies
- Genetic manipulation to assess SNX16 function in ACR
- Investigating interactions between SNX16, Rab GTPases, and mTORC1
Main Results:
- SNX16 identified as a crucial component of the recycler complex at autolysosomes.
- SNX16 regulates recycler complex formation, cargo recognition, and links STX17-SNX4-SNX5 to dynein-dynactin.
- SNX16-cargo interactions are modulated by Rab32 and Rab38.
- mTORC1 phosphorylates SNX16, inhibiting ACR by preventing recycler complex assembly.
Conclusions:
- SNX16 is a novel component of the recycler complex essential for ACR.
- mTORC1 signaling directly regulates ACR through SNX16 phosphorylation, linking nutrient sensing to autophagic recycling.
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