Abstract
Temperature potently modulates various physiologic processes including organismal motility, growth rate, reproduction, and ageing. In ectotherms, longevity varies inversely with temperature, with animals living shorter at higher temperatures. Thermal effects on lifespan and other processes are ascribed to passive changes in metabolic rate, but recent evidence also suggests a regulated process. Here, we demonstrate that in response to temperature, daf-41/ZC395.10, the C. elegans homolog of p23 co-chaperone/prostaglandin E synthase-3, governs entry into the long-lived dauer diapause and regulates adult lifespan. daf-41 deletion triggers constitutive entry into the dauer diapause at elevated temperature dependent on neurosensory machinery (daf-10/IFT122), insulin/IGF-1 signaling (daf-16/FOXO), and steroidal signaling (daf-12/FXR). Surprisingly, daf-41 mutation alters the longevity response to temperature, living longer than wild-type at 25°C but shorter than wild-type at 15°C. Longevity phenotypes at 25°C work through daf-16/FOXO and heat shock factor hsf-1, while short lived phenotypes converge on daf-16/FOXO and depend on the daf-12/FXR steroid receptor. Correlatively daf-41 affected expression of DAF-16 and HSF-1 target genes at high temperature, and nuclear extracts from daf-41 animals showed increased occupancy of the heat shock response element. Our studies suggest that daf-41/p23 modulates key transcriptional changes in longevity pathways in response to temperature.
Highlights
Temperature dramatically impacts the lifespan of ectotherms, with lower temperatures typically extending and higher temperatures shortening life [1,2,3]
Deletion of p23 results in animals that are long lived at high temperatures and short lived at low temperatures relative to normal wild type animals
Our experiments indicate that p23 regulates lifespan through the neurosensory apparatus
Summary
Temperature is a critical environmental factor that affects ageing in both cold-blooded and warm-blooded species. Lifespan varies inversely with temperature, with higher temperature resulting in faster development but shorter lifespan. This phenomenon has been usually attributed to passive changes in metabolic rate, but recent work suggests that this process is regulated. Our experiments indicate that p23 regulates lifespan through the neurosensory apparatus These in turn impinge on key longevity regulators that mediate the transcriptional outputs of insulin/IGF, heat shock response and steroidal signaling. These studies suggest that complexes formed by p23 play a central role in regulating longevity in response to temperature
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