The cAMP-PKA pathway-mediated fat mobilization is required for cold tolerance in C. elegans

Abstract 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 t...

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Autores principales: Fang Liu, Yi Xiao, Xing-Lai Ji, Ke-Qin Zhang, Cheng-Gang Zou
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Lenguaje:EN
Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/6087771228924ea292d5390969396283
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spelling oai:doaj.org-article:6087771228924ea292d53909693962832021-12-02T12:31:58ZThe cAMP-PKA pathway-mediated fat mobilization is required for cold tolerance in C. elegans10.1038/s41598-017-00630-w2045-2322https://doaj.org/article/6087771228924ea292d53909693962832017-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-00630-whttps://doaj.org/toc/2045-2322Abstract 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.Fang LiuYi XiaoXing-Lai JiKe-Qin ZhangCheng-Gang ZouNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Fang Liu
Yi Xiao
Xing-Lai Ji
Ke-Qin Zhang
Cheng-Gang Zou
The cAMP-PKA pathway-mediated fat mobilization is required for cold tolerance in C. elegans
description Abstract 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.
format article
author Fang Liu
Yi Xiao
Xing-Lai Ji
Ke-Qin Zhang
Cheng-Gang Zou
author_facet Fang Liu
Yi Xiao
Xing-Lai Ji
Ke-Qin Zhang
Cheng-Gang Zou
author_sort Fang Liu
title The cAMP-PKA pathway-mediated fat mobilization is required for cold tolerance in C. elegans
title_short The cAMP-PKA pathway-mediated fat mobilization is required for cold tolerance in C. elegans
title_full The cAMP-PKA pathway-mediated fat mobilization is required for cold tolerance in C. elegans
title_fullStr The cAMP-PKA pathway-mediated fat mobilization is required for cold tolerance in C. elegans
title_full_unstemmed The cAMP-PKA pathway-mediated fat mobilization is required for cold tolerance in C. elegans
title_sort camp-pka pathway-mediated fat mobilization is required for cold tolerance in c. elegans
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/6087771228924ea292d5390969396283
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