Regulation of the longevity response to temperature by thermosensory neurons in Caenorhabditis elegans.
Regulation of the longevity response to temperature by thermosensory neurons in Caenorhabditis elegans.
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DOI：
10.1016/j.cub.2009.03.041
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发表时间：
2009-05-12
期刊：
影响因子：
--
通讯作者：
Kenyon C
中科院分区：
文献类型：
--
作者：
Lee SJ;Kenyon C
许多变温动物，包括线虫，在高温下的寿命比在低温下短。人们普遍认为高温仅通过影响化学反应速率来缩短变温动物的寿命。在这项研究中，我们对这种观点提出了质疑，并询问寿命的温度依赖性是否受到主动调节。我们证明热感觉神经元在寿命的温度依赖性中发挥调节作用。热感觉所需的基因失活，或激光消融热感觉神经元，会导致动物在温暖的温度下寿命更短。我们发现热感应突变会降低 daf-9 的表达，daf-9 是合成抑制 DAF-12/核激素受体的配体所需的基因。此外，我们还发现，热敏突变体在温暖温度下的短暂寿命被 daf-12(−) 突变完全抑制。我们的数据表明，热感觉神经元通过改变类固醇信号通路的活性来影响温暖温度下的寿命，从而影响寿命。我们认为，这种热感应系统使秀丽隐杆线虫能够减少温暖的温度对衰老过程的影响，而温血动物通过控制温度本身来做到这一点。
Many ectotherms, including C. elegans, have shorter lifespans at high temperature than at low temperature. High temperature is generally thought to decrease the lifespan of ectotherms simply through its effects on chemical reaction rates. In this study, we questioned this view and asked whether the temperature-dependence of lifespan is subject to active regulation. We show that thermosensory neurons play a regulatory role in the temperature dependence of lifespan. Inactivation of genes required for thermosensation, or laser ablation of thermosensory neurons, causes animals to have even shorter lifespans at warm temperature. We find that thermosensory mutations decrease expression of daf-9, a gene required for the synthesis of ligands that inhibit the DAF-12/nuclear hormone receptor. In addition, we show that the short lifespan of thermosensory mutants at warm temperature is completely suppressed by a daf-12(−) mutation. Our data suggest that thermosensory neurons affect lifespan at warm temperature by changing the activity of a steroid signaling pathway which in turn affects longevity. We propose that this thermosensory system allows C. elegans to reduce the effect that warm temperature would otherwise have on processes that affect aging, something that warm-blooded animals do by controlling temperature itself.
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