Glucose starvation inhibits autophagy via vacuolar hydrolysis and induces plasma membrane internalization by down regulating recycling [Membrane Biology]

April 21st, 2014 by Lang, M. J., Martinez-Marquez, J. Y., Prosser, D. C., Ganser, L. R., Buelto, D., Wendland, B., Duncan, M. C.

Cellular energy influences all aspects of cellular function. Although cells can adapt to a gradual reduction in energy, acute energy depletion poses a unique challenge. Because acute depletion hampers the transport of new energy sources into the cell, the cell must use endogenous substrates to replenish energy after acute depletion. In the yeast Saccharomyces cerevisiae, glucose starvation causes an acute depletion of intracellular energy that recovers during continued glucose starvation. However, how the cell replenishes energy during the early phase of glucose starvation is unknown. In this study, we investigate the role of pathways that deliver proteins and lipids to the vacuole during glucose starvation. We report that in response to glucose starvation, plasma membrane proteins are directed to the vacuole through reduced recycling at the endosomes. Furthermore, we find that vacuolar hydrolysis inhibits macroautophagy in a target of rapamycin complex 1 (TORC1) dependent manner. Accordingly, we find that endocytosis and hydrolysis are required for survival in glucose starvation, whereas macroautophagy is dispensable. Together these results suggest that hydrolysis of components delivered to the vacuole independent of autophagy is the cell survival mechanism used by Saccharomyces cerevisiae in response to glucose starvation.
  • Posted in Journal of Biological Chemistry, Publications
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