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PLoS One. 2012;7(9):e44720. doi: 10.1371/journal.pone.0044720. Epub 2012 Sep 6.

Metabolic rate regulates L1 longevity in C. elegans.

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1
Departments of Biochemistry and Molecular Biology, Virginia Commonwealth University, Richmond, Virginia, United States of America.

Abstract

Animals have to cope with starvation. The molecular mechanisms by which animals survive long-term starvation, however, are not clearly understood. When they hatch without food, C. elegans arrests development at the first larval stage (L1) and survives more than two weeks. Here we show that the survival span of arrested L1s, which we call L1 longevity, is a starvation response regulated by metabolic rate during starvation. A high rate of metabolism shortens the L1 survival span, whereas a low rate of metabolism lengthens it. The longer worms are starved, the slower they grow once they are fed, suggesting that L1 arrest has metabolic costs. Furthermore, mutants of genes that regulate metabolism show altered L1 longevity. Among them, we found that AMP-dependent protein kinase (AMPK), as a key energy sensor, regulates L1 longevity by regulating this metabolic arrest. Our results suggest that L1 longevity is determined by metabolic rate and that AMPK as a master regulator of metabolism controls this arrest so that the animals survive long-term starvation.

PMID:
22970296
PMCID:
PMC3435313
DOI:
10.1371/journal.pone.0044720
[Indexed for MEDLINE]
Free PMC Article
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