Regulation of the Longevity Response to Temperature by Thermosensory Neurons in Caenorhabditis elegans

• Published in: Current biology Vol. 19; no. 9; pp. 715 - 722
• Main Authors: Lee, Seung-Jae, Kenyon, Cynthia
• Format: Journal Article
• Language: English
• Published: England Elsevier Inc 12-05-2009
• Subjects: Aging; Animals; Caenorhabditis elegans; Caenorhabditis elegans - physiology; Caenorhabditis elegans Proteins - genetics; Caenorhabditis elegans Proteins - metabolism; CELLBIO; Cytochrome P-450 Enzyme System - metabolism; Data processing; DEVBIO; DNA Primers - genetics; Gene Expression Regulation - genetics; Gene Expression Regulation - physiology; Lasers; Life span; Longevity; Longevity - physiology; Microscopy, Fluorescence; MOLNEURO; Mutation; Mutation - genetics; Nerve Tissue Proteins - genetics; Neurons; Nuclear receptors; Reverse Transcriptase Polymerase Chain Reaction; Temperature; Temperature effects; Thermoreceptors - physiology; CELLBIO; DEVBIO; MOLNEURO
• ISSN: 0960-9822; 1879-0445
• DOI: 10.1016/j.cub.2009.03.041

Many ectotherms, including
C. elegans, have shorter life spans at high temperature than at low temperature. High temperature is generally thought to increase the “rate of living” simply by increasing chemical reaction rates. In this study, we questioned this view and asked whether the temperature dependence of life span is subject to active regulation.
We show that thermosensory neurons play a regulatory role in the temperature dependence of life span. Surprisingly, inhibiting the function of thermosensory neurons by mutation or laser ablation causes animals to have even shorter life spans at warm temperature. Thermosensory mutations shorten life span by decreasing expression of
daf-9, a gene required for the synthesis of ligands that inhibit the DAF-12, a nuclear hormone receptor. The short life span of thermosensory mutants at warm temperature is completely suppressed by a
daf-12(-) mutation.
Our data suggest that thermosensory neurons affect life span at warm temperature by changing the activity of a steroid-signaling pathway that 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.