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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Nature Portfolio
2017
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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) |
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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 |
work_keys_str_mv |
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