A C-ELEGANS MUTANT THAT LIVES TWICE AS LONG AS WILD-TYPE
A C-ELEGANS MUTANT THAT LIVES TWICE AS LONG AS WILD-TYPE
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DOI：
10.1038/366461a0
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发表时间：
1993-12-02
期刊：
影响因子：
64.8
通讯作者：
TABTIANG, R
中科院分区：
文献类型：
--
作者：
KENYON, C;CHANG, J;TABTIANG, R
我们已经发现daf-2基因的突变可以导致可育的、活跃的、成年的秀丽隐杆线虫雌雄同体的寿命是野生型的两倍多。这种在任何生物体中被报道的最长的寿命延长需要第二个基因daf-16的活性。这两种基因也调节着幼虫的形成，这是一种发育受阻的幼虫形式，由拥挤和饥饿诱导，寿命很长。我们的研究结果提出了一种可能性，即道尔的长寿不仅仅是其生长受阻的结果，而是一种受调节的寿命延长机制的结果，这种机制可以与道尔形成的其他方面分离。Daf-2和daf-16为理解如何延长寿命提供了切入点。
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.