Staying alive: metabolic adaptations to quiescence

Cell Cycle. 2012 May 1;11(9):1680-96. doi: 10.4161/cc.19879. Epub 2012 May 1.

Abstract

Quiescence is a state of reversible cell cycle arrest that can grant protection against many environmental insults. In some systems, cellular quiescence is associated with a low metabolic state characterized by a decrease in glucose uptake and glycolysis, reduced translation rates and activation of autophagy as a means to provide nutrients for survival. For cells in multiple different quiescence model systems, including Saccharomyces cerevisiae, mammalian lymphocytes and hematopoietic stem cells, the PI3Kinase/TOR signaling pathway helps to integrate information about nutrient availability with cell growth rates. Quiescence signals often inactivate the TOR kinase, resulting in reduced cell growth and biosynthesis. However, quiescence is not always associated with reduced metabolism; it is also possible to achieve a state of cellular quiescence in which glucose uptake, glycolysis and flux through central carbon metabolism are not reduced. In this review, we compare and contrast the metabolic changes that occur with quiescence in different model systems.

Publication types

  • Review

MeSH terms

  • Adaptation, Physiological*
  • Animals
  • Autophagy
  • Cell Cycle Checkpoints*
  • Cell Proliferation
  • Escherichia coli / cytology
  • Escherichia coli / metabolism*
  • Fibroblasts / cytology
  • Fibroblasts / metabolism
  • Glucose / metabolism
  • Glycolysis
  • Hematopoietic Stem Cells / cytology
  • Hematopoietic Stem Cells / metabolism*
  • Humans
  • Lymphocyte Activation
  • Phosphatidylinositol 3-Kinase / metabolism
  • Saccharomyces cerevisiae / cytology
  • Saccharomyces cerevisiae / metabolism*
  • Signal Transduction
  • T-Lymphocytes / cytology
  • T-Lymphocytes / metabolism
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • Phosphatidylinositol 3-Kinase
  • TOR Serine-Threonine Kinases
  • Glucose