Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Mech Ageing Dev. 2006 May;127(5):458-72. Epub 2006 Mar 7.

Diapause-associated metabolic traits reiterated in long-lived daf-2 mutants in the nematode Caenorhabditis elegans.

Author information

  • 1Department of Biology, University College London, UK.

Erratum in

  • Mech Ageing Dev. 2006;127(12):922.

Corrected and republished in

Abstract

The longevity of the Caenorhabditis elegans diapausal dauer larva greatly exceeds that of the adult. Dauer formation and adult ageing are both regulated by insulin/IGF-1 signaling (IIS). Reduced IIS, e.g. by mutation of the daf-2 insulin/IGF-1 receptor gene, increases adult lifespan. This may reflect mis-expression in the adult of dauer longevity-assurance processes. Since IIS plays a central role in the regulation of metabolism, metabolic alterations shared by dauer larvae and daf-2 adults represent candidate mechanisms for lifespan determination. We have conducted a detailed comparison of transcript profile data from dauers and daf-2 mutant adults, focusing on expression of metabolic pathway genes. Our results imply up-regulation in both dauers and daf-2 mutant adults of gluconeogenesis, glyoxylate pathway activity, and trehalose biosynthesis. Down-regulation of the citric acid cycle and mitochondrial respiratory chain occurs in dauers, but not daf-2 adults. However, the F(1) ATPase inhibitor was up-regulated in both, implying enhanced homeostasis in conditions where mitochondria are stressed. Overall, the data implies increased conversion of fat to carbohydrate, and conservation of ATP stocks in daf-2 mutant adults, suggesting a state of increased energy availability. We postulate that this fuels increased somatic maintenance activity, as suggested by the disposable soma theory.

PMID:
16522328
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk