Abstract

The wild-type Caenorhabditis elegans nematode ages rapidly, undergoing development, senescence, and death in less than 3 weeks. In contrast, mutants with reduced activity of the gene daf-2, a homolog of the insulin and insulin-like growth factor receptors, age more slowly than normal and live more than twice as long. These mutants are active and fully fertile and have normal metabolic rates. The life-span extension caused by daf-2 mutations requires the activity of the gene daf-16. daf-16 appears to play a unique role in life-span regulation and encodes a member of the hepatocyte nuclear factor 3 (HNF-3)/forkhead family of transcriptional regulators. In humans, insulin down-regulates the expression of certain genes by antagonizing the activity of HNF-3, raising the possibility that aspects of this regulatory system have been conserved.

Keywords

Caenorhabditis elegansBiologyMutantGeneCell biologyGeneticsCaenorhabditisFunction (biology)Senescence

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Publication Info

Year
1997
Type
article
Volume
278
Issue
5341
Pages
1319-1322
Citations
1483
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Closed

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Kui Lin, Jennie B. Dorman, Aylin R. Rodan et al. (1997). <i>daf-16</i> : An HNF-3/forkhead Family Member That Can Function to Double the Life-Span of <i>Caenorhabditis elegans</i>. Science , 278 (5341) , 1319-1322. https://doi.org/10.1126/science.278.5341.1319

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DOI
10.1126/science.278.5341.1319