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Induction of autophagy supports the bioenergetic demands of quiescent muscle stem cell activation
Author(s) -
Tang Ann H,
Rando Thomas A
Publication year - 2014
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201488278
Subject(s) - autophagy , bioenergetics , biology , microbiology and biotechnology , proteostasis , intracellular , flux (metallurgy) , biochemistry , mitochondrion , chemistry , apoptosis , organic chemistry
The exit of a stem cell out of quiescence into an activated state is characterized by major metabolic changes associated with increased biosynthesis of proteins and macromolecules. The regulation of this transition is poorly understood. Using muscle stem cells, or satellite cells ( SC s), we found that autophagy, which catabolizes intracellular contents to maintain proteostasis and to produce energy during nutrient deprivation, was induced during SC activation. Inhibition of autophagy suppressed the increase in ATP levels and delayed SC activation, both of which could be partially rescued by exogenous pyruvate as an energy source, suggesting that autophagy may provide nutrients necessary to meet bioenergetic demands during this critical transition from quiescence to activation. We found that SIRT 1, a known nutrient sensor, regulates autophagic flux in SC progeny. A deficiency of SIRT 1 led to a delay in SC activation that could also be partially rescued by exogenous pyruvate. These studies suggest that autophagy, regulated by SIRT 1, may play an important role during SC activation to meet the high bioenergetic demands of the activation process.