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mTOR signalling

AMPK knocks at the gate of GATOR

Nature Metabolism volume 5, pages 197–198 (2023)Cite this article

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Dai and colleagues show that activation of AMPK by glucose starvation leads to phosphorylation of GATOR2 and affects nutrient-dependent activation of mTORC1.

Our cells react with a repertoire of tightly regulated responses to fluctuations in the availability of nutrients and energy. Rates of build-up and breakdown of cellular biomass are tuned to adapt to abundance and scarcity. Among the critical players that couple nutrient and energy sufficiency to the execution of anabolic versus catabolic functions in the cell are the AMP-activated protein kinase (AMPK) and the mechanistic target of rapamycin complex 1 (mTORC1).

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Fig. 1: GATOR2 is phosphorylated by AMPK in response to glucose starvation, suppressing mTORC1 activation.

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Acknowledgements

A.E. laboratory acknowledges funding by a RETOS Projects Program of the Spanish Ministry of Science, Innovation and Universities, the Spanish State Research Agency (AEI/10.13039 /501100011033) co-funded by the European Regional Development Fund (PID2019-104012RB-I00), a FERO Grant for Research in Oncology and the LaCaixa Banking Foundation (LCF/PR/HR21/0046). A.E. is an EMBO Young Investigator.

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  1. Spanish National Cancer Research Center, Madrid, Spain

    Nerea Deleyto-Seldas & Alejo Efeyan

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  1. Nerea Deleyto-Seldas
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  2. Alejo Efeyan
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N.D.-S. and A.E. wrote and edited the text and figure.

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Correspondence to Alejo Efeyan.

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The authors declare no competing interests.

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Deleyto-Seldas, N., Efeyan, A. AMPK knocks at the gate of GATOR. Nat Metab 5, 197–198 (2023). https://doi.org/10.1038/s42255-022-00729-z

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