The G protein‐coupled receptor (GPCR) encoding family of genes constitutes more than 6% of genes in Caenorhabditis elegans genome. GPCRs control behavior, innate immunity, chemotaxis, and food search behavior. Here, we show that C. elegans longevity is regulated by a chemosensory GPCR STR‐2, expressed in AWC and ASI amphid sensory neurons. STR‐2 function is required at temperatures of 20°C and higher on standard Escherichia coli OP50 diet. Under these conditions, this neuronal receptor also controls health span parameters and lipid droplet (LD) homeostasis in the intestine. We show that STR‐2 regulates expression of delta‐9 desaturases, fat‐5, fat‐6 and fat‐7, and of diacylglycerol acyltransferase dgat‐2. Rescue of the STR‐2 function in either AWC and ASI, or ASI sensory neurons alone, restores expression of fat‐5, dgat‐2 and restores LD stores and longevity. Rescue of stored fat levels of GPCR mutant animals to wild‐type levels, with low concentration of glucose, rescues its lifespan phenotype. In all, we show that neuronal STR‐2 GPCR facilitates control of neutral lipid levels and longevity in C. elegans.

中文翻译：

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STR-2 G蛋白偶联受体对脂质代谢的神经元控制可延长秀丽隐杆线虫的寿命。

秀丽隐杆线虫基因组中编码基因家族的G蛋白偶联受体（GPCR）占6％以上。GPCR控制行为，先天免疫，趋化性和食物搜寻行为。在这里，我们显示秀丽隐杆线虫的寿命受化学感应GPCR STR-2调控，在AWC和ASI肢体感觉神经元中表达。标准大肠杆菌OP50饮食在20°C或更高温度下需要STR-2功能。在这种情况下，该神经元受体还控制着健康跨度参数和肠道中的脂质滴（LD）稳态。我们显示STR-2调节delta-9脱氢酶，fat-5，fat-6和fat-7的表达，以及二酰基甘油酰基转移酶dgat-2。在AWC和ASI或仅ASI感觉神经元中挽救STR-2功能，可恢复fat-5，dgat-2的表达并恢复LD的储存和寿命。GPCR突变体动物体内储存的脂肪水平降低至野生型水平，且葡萄糖浓度低，可以挽救其寿命表型。总之，我们表明神经元STR-2 GPCR有助于控制秀丽隐杆线虫的中性脂质水平和寿命。