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AMPK and vacuole-associated Atg14p orchestrate μ-lipophagy for energy production and long-term survival under glucose starvation

  • Author(s): Seo, AY
  • Lau, PW
  • Feliciano, D
  • Sengupta, P
  • Le Gros, MA
  • Cinquin, B
  • Larabell, CA
  • Lippincott-Schwartz, J
  • et al.
Abstract

© Seo et al. Dietary restriction increases the longevity of many organisms, but the cell signaling and organellar mechanisms underlying this capability are unclear. We demonstrate that to permit long-term survival in response to sudden glucose depletion, yeast cells activate lipid-droplet (LD) consumption through micro-lipophagy (μ-lipophagy), in which fat is metabolized as an alternative energy source. AMP-activated protein kinase (AMPK) activation triggered this pathway, which required Atg14p. More gradual glucose starvation, amino acid deprivation or rapamycin did not trigger μ-lipophagy and failed to provide the needed substitute energy source for long-term survival. During acute glucose restriction, activated AMPK was stabilized from degradation and interacted with Atg14p. This prompted Atg14p redistribution from ER exit sites onto liquidordered vacuole membrane domains, initiating μ-lipophagy. Our findings that activated AMPK and Atg14p are required to orchestrate μ-lipophagy for energy production in starved cells is relevant for studies on aging and evolutionary survival strategies of different organisms.

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