The longevity response to warm temperature is neurally controlled via regulation of collagen genes

Lower temperatures have been associated with longer lifespan, while higher temperatures with shorter lifespan. These inverse effects of temperature on longevity were traditionally explained by the "rate of living theory", which posits that higher temperatures increase chemical reaction rates, thus speeding up the aging process. Recent studies have identified specific molecules and cells that mediate the longevity response to temperature, suggesting that the temperature effects on aging are not simply thermodynamic but regulated processes. However, the mechanisms underlying such regulation are not well understood. In the current study, we found that Caenorhabditis elegans lacking NPR-8, a neuronal GPCR related to the mammalian neuropeptide Y receptors, exhibited extended lifespan at warm temperature. Such lifespan extension can be suppressed by re-expression of NPR-8 in the amphid sensory neurons AWB and AWC or by inactivation of NPR-8-regulated collagen genes. These results suggest that the warm temperature effect on longevity is regulated by the nervous system through controlling collagen gene expression. Our study potentially provides mechanistic insights into understanding the relationship between temperature and longevity, which could prove useful in mitigating negative impacts of increasing temperature due to global warming.