State key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, School of Life Sciences, Yunnan University, Kunming, Yunnan, 650091, China.
Faculty of Basic Medicine, Kunming Medical University, Kunming, Yunnan, 650031, China.
Nat Commun. 2019 Jun 13;10(1):2602. doi: 10.1038/s41467-019-10475-8.
Temperature is a key factor for determining the lifespan of both poikilotherms and homeotherms. It is believed that animals live longer at lower body temperatures. However, the precise mechanism remains largely unknown. Here, we report that autophagy serves as a boost mechanism for longevity at low temperature in the nematode Caenorhabditis elegans. The adiponectin receptor AdipoR2 homolog PAQR-2 signaling detects temperature drop and augments the biosynthesis of two ω-6 polyunsaturated fatty acids, γ-linolenic acid and arachidonic acid. These two polyunsaturated fatty acids in turn initiate autophagy in the epidermis, delaying an age-dependent decline in collagen contents, and extending the lifespan. Our findings reveal that the adiponectin receptor PAQR-2 signaling acts as a regulator linking low temperature with autophagy to extend lifespan, and suggest that such a mechanism may be evolutionally conserved among diverse organisms.
温度是决定变温动物和恒温动物寿命的关键因素。人们认为,动物的体温越低,寿命就越长。然而,其确切的机制在很大程度上仍然未知。在这里,我们报告说,自噬是线虫秀丽隐杆线虫在低温下延长寿命的促进机制。脂联素受体 AdipoR2 同源物 PAQR-2 信号检测到温度下降,并增强了两种 ω-6 多不饱和脂肪酸 γ-亚麻酸和花生四烯酸的生物合成。这两种多不饱和脂肪酸反过来又在表皮中引发自噬,延缓了随年龄增长胶原蛋白含量的下降,并延长了寿命。我们的研究结果表明,脂联素受体 PAQR-2 信号作为一种调节剂,将低温与自噬联系起来,以延长寿命,并表明这种机制可能在不同的生物体中是进化保守的。