Regulatory mechanism of cold-inducible diapause in Caenorhabditis elegans

Makoto Horikawa (), Masamitsu Fukuyama, Adam Antebi and Masaki Mizunuma ()
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Makoto Horikawa: Graduate School of Integrated Sciences for Life, Hiroshima University
Masamitsu Fukuyama: Graduate School of Pharmaceutical Sciences, University of Tokyo
Adam Antebi: Max Planck Institute for Biology of Ageing
Masaki Mizunuma: Graduate School of Integrated Sciences for Life, Hiroshima University

Nature Communications, 2024, vol. 15, issue 1, 1-18

Abstract: Abstract Temperature is a critical environmental cue that controls the development and lifespan of many animal species; however, mechanisms underlying low-temperature adaptation are poorly understood. Here, we describe cold-inducible diapause (CID), another type of diapause induced by low temperatures in Caenorhabditis elegans. A premature stop codon in heat shock factor 1 (hsf-1) triggers entry into CID at 9 °C, whereas wild-type animals enter CID at 4 °C. Furthermore, both wild-type and hsf-1(sy441) mutant animals undergoing CID can survive for weeks, and resume growth at 20 °C. Using epistasis analysis, we demonstrate that neural signalling pathways, namely tyraminergic and neuromedin U signalling, regulate entry into CID of the hsf-1 mutant. Overexpression of anti-ageing genes, such as hsf-1, XBP1/xbp-1, FOXO/daf-16, Nrf2/skn-1, and TFEB/hlh-30, also inhibits CID entry of the hsf-1 mutant. Based on these findings, we hypothesise that regulators of the hsf-1 mutant CID may impact longevity, and successfully isolate 16 long-lived mutants among 49 non-CID mutants via genetic screening. Furthermore, we demonstrate that the nonsense mutation of MED23/sur-2 prevents CID entry of the hsf-1(sy441) mutant and extends lifespan. Thus, CID is a powerful model to investigate neural networks involving cold acclimation and to explore new ageing mechanisms.

Date: 2024
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DOI: 10.1038/s41467-024-50111-8

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