daf-16 Protects the Nematode Caenorhabditis elegans During Food Deprivation

Inhibition of either the insulin-like or target of rapamycin (TOR) pathways in the nematode Caenorhabditis elegans extends life span. Here, we demonstrate that starvation and inhibition of the C. elegans insulin receptor homolog (daf-2) elicits a daf-16-dependent up-regulation of a mitochondrial sup...

Full description

Saved in:
Bibliographic Details
Published in:The journals of gerontology. Series A, Biological sciences and medical sciences Biological sciences and medical sciences, 2006-05, Vol.61 (5), p.444-460
Main Authors: Henderson, Samuel T., BonafeĢ€, Massimiliano, Johnson, Thomas E.
Format: Article
Language:English
Subjects:
Adaptation, Physiological
Amino acids
Animals
Base Sequence
Blotting, Western
Caenorhabditis elegans - physiology
Caenorhabditis elegans Proteins - genetics
Caenorhabditis elegans Proteins - metabolism
Disease Models, Animal
Down-Regulation
Food Deprivation
Forkhead Transcription Factors
Life expectancy
Molecular Sequence Data
Mutation
Nematodes
Oxidative Stress
Polymerase Chain Reaction
Protein synthesis
Reactive Oxygen Species - metabolism
Ribonucleic acid
RNA
Sensitivity and Specificity
Transcription Factors - genetics
Transcription Factors - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Inhibition of either the insulin-like or target of rapamycin (TOR) pathways in the nematode Caenorhabditis elegans extends life span. Here, we demonstrate that starvation and inhibition of the C. elegans insulin receptor homolog (daf-2) elicits a daf-16-dependent up-regulation of a mitochondrial superoxide dismutase (sod-3). We also find that although heat and oxidative stress result in nuclear localization of the DAF-16 protein, these stressors do not activate a SOD-3 reporter, suggesting that nuclear localization alone may not be sufficient for transcriptional activation of DAF-16. We show that inhibition of either TOR activity or key components of the cognate translational machinery (eIF-4G and EIF-2B homologs) increases life span by both daf-16-dependent and -independent mechanisms. Finally, we demonstrate that at least one nematode hexokinase is localized to the mitochondria. We propose that the increased life spans conferred by alterations in both the TOR and insulin-like pathways function by inappropriately activating food-deprivation pathways.
ISSN:1079-5006
1758-535X
DOI:10.1093/gerona/61.5.444