Journal
SCIENTIFIC REPORTS
Volume 7, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-017-00630-w
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Funding
- NIH Office of Research Infrastructure Programs [P40 OD010440]
- National Basic Research Program of China [2013CB127500, 2012CB722208]
- National Natural Science Foundation of China [311171365]
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Low temperature has a great impact on animal life. Homoiotherms such as mammals increase their energy expenditure to produce heat by activating the cAMP- protein kinase A ( PKA)- hormone- sensitive lipase ( HSL) pathway under cold stress. Although poikilothermic animals do not have the ability to regulate body temperature, whether this pathway is required for cold tolerance remains unknown. We have now achieved this using the genetically tractable model animal Caenorhabditis elegans. We demonstrate that cold stress activates PKA signaling, which in turn up- regulates the expression of a hormone- sensitive lipase hosl- 1. The lipase induces fat mobilization, leading to glycerol accumulation, thereby protecting worms against cold stress. Our findings provide an example of an evolutionarily conserved mechanism for cold tolerance that has persisted in both poikilothermic and homoeothermic animals.
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