Regulation of C-elegans life-span by insulinlike signaling in the nervous system
Regulation of C-elegans life-span by insulinlike signaling in the nervous system
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DOI：
10.1126/science.290.5489.147
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发表时间：
2000-10-06
期刊：
影响因子：
56.9
通讯作者：
Ruvkun, G
中科院分区：
文献类型：
--
作者：
Wolkow, CA;Kimura, KD;Ruvkun, G
胰岛素样信号通路控制秀丽线虫的衰老。新陈代谢和发育。Daf-2胰岛素受体类基因或下游AGE-1磷脂酰肌醇3-激酶基因的突变可使成年人的寿命延长两到三倍。为了确定这一途径调节衰老和新陈代谢的组织，我们恢复了daf-2途径只向神经元、肌肉或肠道发送信号。仅神经元中的胰岛素样信号就足以确定野生型寿命，但肌肉或肠道信号不足以确定。然而，恢复对肌肉的daf-2信号通路可以挽救代谢缺陷，从而使寿命和新陈代谢的调节脱钩。这些发现表明，神经系统是动物长寿的中心调节器。
An insulinlike signaling pathway controls Caenorhabditis elegans aging. metabolism, and development. Mutations in the daf-2 insulin receptor-like gene or the downstream age-1 phosphoinositide 3-kinase gene extend adult life-span by two- to threefold. To identify tissues where this pathway regulates aging and metabolism, we restored daf-2 pathway signaling to only neurons, muscle, or intestine. Insulinlike signaling in neurons alone was sufficient to specify wild-type life-span, but muscle or intestinal signaling was not. However, restoring daf-2 pathway signaling to muscle rescued metabolic defects, thus decoupling regulation of life-span and metabolism. These findings point to the nervous system as a central regulator of animal longevity.