Kenyon C, Chang J, Gensch E, Rudner A, Tabtiang R
Department of Biochemistry and Biophysics, University of California at San Francisco 94143-0554.
Nature. 1993 Dec 2;366(6454):461-4. doi: 10.1038/366461a0.
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 organism, 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-lived. 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.
我们发现,基因daf-2中的突变可使可育、活跃的成年秀丽隐杆线虫雌雄同体的寿命比野生型延长两倍多。这种寿命延长是迄今为止在任何生物体中报道的最长的,它需要第二个基因daf-16的活性。这两个基因还调节滞育幼虫的形成,滞育幼虫是一种发育停滞的幼虫形态,由拥挤和饥饿诱导,寿命很长。我们的发现提出了一种可能性,即滞育幼虫的长寿不仅仅是其生长停滞的结果,而是源于一种可与滞育形成的其他方面解耦的受调控的寿命延长机制。daf-2和daf-16为理解如何延长寿命提供了切入点。