Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41467-017-00369-y
Title: Glutamine metabolism regulates autophagy-dependent mTORC1 reactivation during amino acid starvation
Authors: Tan, H.W.S 
Sim, A.Y.L 
Long, Y.C 
Keywords: amino acid
autophagy related protein 5
glutamine
mammalian target of rapamycin complex 1
animal
autophagy
cell culture
cell line
cytology
fibroblast
genetics
Hep-G2 cell line
human
immunoblotting
knockout mouse
lysosome
mammalian embryo
metabolism
myoblast
Amino Acids
Animals
Autophagy
Autophagy-Related Protein 5
Cell Line
Cells, Cultured
Embryo, Mammalian
Fibroblasts
Glutamine
Hep G2 Cells
Humans
Immunoblotting
Lysosomes
Mechanistic Target of Rapamycin Complex 1
Mice, Knockout
Myoblasts
Issue Date: 2017
Publisher: Nature Publishing Group
Citation: Tan, H.W.S, Sim, A.Y.L, Long, Y.C (2017). Glutamine metabolism regulates autophagy-dependent mTORC1 reactivation during amino acid starvation. Nature Communications 8 (1) : 338. ScholarBank@NUS Repository. https://doi.org/10.1038/s41467-017-00369-y
Abstract: Activation of autophagy and elevation of glutamine synthesis represent key adaptations to maintain amino acid balance during starvation. In this study, we investigate the role of autophagy and glutamine on the regulation of mTORC1, a critical kinase that regulates cell growth and proliferation. We report that supplementation of glutamine alone is sufficient to restore mTORC1 activity during prolonged amino acid starvation. Inhibition of autophagy abolishes the restorative effect of glutamine, suggesting that reactivation of mTORC1 is autophagy-dependent. Inhibition of glutaminolysis or transamination impairs glutamine-mediated mTORC1 reactivation, suggesting glutamine reactivates mTORC1 specifically through its conversion to glutamate and restoration of non-essential amino acid pool. Despite a persistent drop in essential amino acid pool during amino acid starvation, crosstalk between glutamine and autophagy is sufficient to restore insulin sensitivity of mTORC1. Thus, glutamine metabolism and autophagy constitute a specific metabolic program which restores mTORC1 activity during amino acid starvation. © 2017 The Author(s).
Source Title: Nature Communications
URI: https://scholarbank.nus.edu.sg/handle/10635/174404
ISSN: 2041-1723
DOI: 10.1038/s41467-017-00369-y
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