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Freeze–thaw Caenorhabditis elegans freeze–thaw stress response is regulated by the insulin/IGF-1 receptor daf-2
BACKGROUND: Adaption to cold temperatures, especially those below freezing, is essential for animal survival in cold environments. Freezing is also used for many medical, scientific, and industrial purposes. Natural freezing survival in animals has been extensively studied. However, the underlying m...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4669615/ https://www.ncbi.nlm.nih.gov/pubmed/26635120 http://dx.doi.org/10.1186/s12863-015-0298-5 |
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author | Hu, Jian-Ping Xu, Xiao-Ying Huang, Li-Ying Wang, Li-shun Fang, Ning-Yuan |
author_facet | Hu, Jian-Ping Xu, Xiao-Ying Huang, Li-Ying Wang, Li-shun Fang, Ning-Yuan |
author_sort | Hu, Jian-Ping |
collection | PubMed |
description | BACKGROUND: Adaption to cold temperatures, especially those below freezing, is essential for animal survival in cold environments. Freezing is also used for many medical, scientific, and industrial purposes. Natural freezing survival in animals has been extensively studied. However, the underlying mechanisms remain unclear. Previous studies demonstrated that animals survive in extremely cold weather by avoiding freezing or controlling the rate of ice-crystal formation in their bodies, which indicates that freezing survival is a passive thermodynamic process. RESULTS: Here, we showed that genetic programming actively promotes freezing survival in Caenorhabditis elegans. We found that daf-2, an insulin/IGF-1 receptor homologue, and loss-of-function enhanced survival during freeze–thaw stress, which required the transcription factor daf-16/FOXO and age-independent target genes. In particular, the freeze–thaw resistance of daf-2(rf) is highly allele-specific and has no correlation with lifespan, dauer formation, or hypoxia stress resistance. CONCLUSIONS: Our results reveal a new function for daf-2 signaling, and, most importantly, demonstrate that genetic programming contributes to freezing survival. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12863-015-0298-5) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4669615 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-46696152015-12-05 Freeze–thaw Caenorhabditis elegans freeze–thaw stress response is regulated by the insulin/IGF-1 receptor daf-2 Hu, Jian-Ping Xu, Xiao-Ying Huang, Li-Ying Wang, Li-shun Fang, Ning-Yuan BMC Genet Research Article BACKGROUND: Adaption to cold temperatures, especially those below freezing, is essential for animal survival in cold environments. Freezing is also used for many medical, scientific, and industrial purposes. Natural freezing survival in animals has been extensively studied. However, the underlying mechanisms remain unclear. Previous studies demonstrated that animals survive in extremely cold weather by avoiding freezing or controlling the rate of ice-crystal formation in their bodies, which indicates that freezing survival is a passive thermodynamic process. RESULTS: Here, we showed that genetic programming actively promotes freezing survival in Caenorhabditis elegans. We found that daf-2, an insulin/IGF-1 receptor homologue, and loss-of-function enhanced survival during freeze–thaw stress, which required the transcription factor daf-16/FOXO and age-independent target genes. In particular, the freeze–thaw resistance of daf-2(rf) is highly allele-specific and has no correlation with lifespan, dauer formation, or hypoxia stress resistance. CONCLUSIONS: Our results reveal a new function for daf-2 signaling, and, most importantly, demonstrate that genetic programming contributes to freezing survival. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12863-015-0298-5) contains supplementary material, which is available to authorized users. BioMed Central 2015-12-03 /pmc/articles/PMC4669615/ /pubmed/26635120 http://dx.doi.org/10.1186/s12863-015-0298-5 Text en © Hu et al. 2015 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Hu, Jian-Ping Xu, Xiao-Ying Huang, Li-Ying Wang, Li-shun Fang, Ning-Yuan Freeze–thaw Caenorhabditis elegans freeze–thaw stress response is regulated by the insulin/IGF-1 receptor daf-2 |
title | Freeze–thaw Caenorhabditis elegans freeze–thaw stress response is regulated by the insulin/IGF-1 receptor daf-2 |
title_full | Freeze–thaw Caenorhabditis elegans freeze–thaw stress response is regulated by the insulin/IGF-1 receptor daf-2 |
title_fullStr | Freeze–thaw Caenorhabditis elegans freeze–thaw stress response is regulated by the insulin/IGF-1 receptor daf-2 |
title_full_unstemmed | Freeze–thaw Caenorhabditis elegans freeze–thaw stress response is regulated by the insulin/IGF-1 receptor daf-2 |
title_short | Freeze–thaw Caenorhabditis elegans freeze–thaw stress response is regulated by the insulin/IGF-1 receptor daf-2 |
title_sort | freeze–thaw caenorhabditis elegans freeze–thaw stress response is regulated by the insulin/igf-1 receptor daf-2 |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4669615/ https://www.ncbi.nlm.nih.gov/pubmed/26635120 http://dx.doi.org/10.1186/s12863-015-0298-5 |
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