HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Henderson, S. T. Articles by Johnson, T. E. PubMed PubMed Citation Articles by Henderson, S. T. Articles by Johnson, T. E.

daf-16 Protects the Nematode Caenorhabditis elegans During Food Deprivation

¹ Institute for Behavioral Genetics, University of Colorado, Boulder.
² Department of Experimental Pathology, and Center for Applied Biomedical Research, University of Bologna, Italy.

Address correspondence to Thomas E. Johnson, PhD, Institute for Behavioral Genetics, Box 447, University of Colorado, Boulder, CO 80309. E-mail: johnsont{at}colorado.edu

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.