Two neurons mediate diet-restriction-induced longevity in C-elegans
Two neurons mediate diet-restriction-induced longevity in C-elegans
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DOI：
10.1038/nature05904
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发表时间：
2007-05-31
期刊：
影响因子：
64.8
通讯作者：
Guarente, Leonard
中科院分区：
文献类型：
--
作者：
Bishop, Nicholas A.;Guarente, Leonard
在许多物种中，饮食限制延长了寿命，延缓了与年龄有关的疾病，并深刻地改变了哺乳动物的内分泌功能。然而，没有任何激素信号在饮食限制的长寿中的因果作用已经得到证实。在这里，我们表明，增加寿命的饮食限制秀丽隐杆线虫需要的转录因子基因skn-1作用于ASIs，一对神经元在头部。饮食限制激活了这两个神经元中的skn-1，它向周围组织发出信号，以增加代谢活动。这些研究结果表明，在饮食限制的后生动物寿命的增加取决于从中央神经元细胞到非神经元体组织的细胞非自主信号传导，并表明ASI神经元通过内分泌机制介导饮食限制诱导的寿命。
Dietary restriction extends lifespan and retards age-related disease in many species and profoundly alters endocrine function in mammals. However, no causal role of any hormonal signal in diet-restricted longevity has been demonstrated. Here we show that increased longevity of diet-restricted Caenorhabditis elegans requires the transcription factor gene skn-1 acting in the ASIs, a pair of neurons in the head. Dietary restriction activates skn-1 in these two neurons, which signals peripheral tissues to increase metabolic activity. These findings demonstrate that increased lifespan in a diet-restricted metazoan depends on cell non-autonomous signalling from central neuronal cells to non-neuronal body tissues, and suggest that the ASI neurons mediate diet-restriction-induced longevity by an endocrine mechanism.