Termination of autophagy and reformation of lysosomes regulated by mTOR

Li Yu, Christina K. McPhee, Lixin Zheng, Gonzalo A. Mardones, Yueguang Rong, Junya Peng, Na Mi, Ying Zhao, Zhihua Liu, Fengyi Wan, Dale W. Hailey, Viola Oorschot, Judith Klumperman, Eric H. Baehrecke and Michael J. Lenardo ()
Additional contact information
Li Yu: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Christina K. McPhee: University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
Lixin Zheng: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Gonzalo A. Mardones: Cell Biology and Metabolism Program, National Institute of Child Health & Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA
Yueguang Rong: School of Life Science, Tsinghua University
Junya Peng: School of Life Science, Tsinghua University
Na Mi: School of Life Science, Tsinghua University
Ying Zhao: Peking University Health Science Center, 38 Xueyuan Road, Beijing 100191, China
Zhihua Liu: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Fengyi Wan: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Dale W. Hailey: Cell Biology and Metabolism Program, National Institute of Child Health & Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA
Viola Oorschot: University Medical Center Utrecht
Judith Klumperman: University Medical Center Utrecht
Eric H. Baehrecke: University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
Michael J. Lenardo: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA

Nature, 2010, vol. 465, issue 7300, 942-946

Abstract: mTOR and autophagy During autophagy, double-membrane autophagosomes sequester intracellular components and then fuse with lysosomes to form autolysosomes in which cargo is degraded. Under starvation conditions, the nutrient-responsive kinase, target of rapamycin (TOR), is inhibited, which results in an induction of autophagy. In this study, Yu et al. report a negative feedback mechanism by which lysosomes are reformed after the termination of autophagy. They demonstrate that upon prolonged starvation conditions, mTOR is reactivated, which attenuates autophagy and results in the formation of tubules and vesicles that extrude from autolysosomes. These mature into functional lysosomes, thereby restoring lysosome numbers in the cell. This feedback mechanism tightly couples nutritional status with the induction and termination of autophagy.

Date: 2010
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DOI: 10.1038/nature09076

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