Abstract
WE have found that mutations in the gene daf-2 can cause fertile, active, adult Caenorhabditis elegans hermaphrodites to live more than twice as long as wild type. This lifespan extension, the largest yet reported in any organism1, requires the activity of a second gene, daf-16. Both genes also regulate formation of the dauer larva, a developmentally arrested larval form that is induced by crowding and starvation and is very long-lived2–4. Our findings raise the possibility that the longevity of the dauer is not simply a consequence of its arrested growth, but instead results from a regulated lifespan extension mechanism that can be uncoupled from other aspects of dauer formation, daf-2 and daf-16 provide entry points into understanding how lifespan can be extended.
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Kenyon, C., Chang, J., Gensch, E. et al. A C. elegans mutant that lives twice as long as wild type. Nature 366, 461–464 (1993). https://doi.org/10.1038/366461a0
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DOI: https://doi.org/10.1038/366461a0
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