Metabolic rate regulates L1 longevity in C. elegans

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

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenylate Kinase / metabolism
  • Animals
  • Caenorhabditis elegans / enzymology
  • Caenorhabditis elegans / metabolism*
  • Caenorhabditis elegans / physiology
  • Energy Metabolism
  • Longevity*
  • Starvation

Substances

  • Adenylate Kinase

Grant support

IL and YY received support from the American Heart Association grant (09SDG2150070). No additional external funding was received for this study. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.