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Thermal stress and mutation accumulation increase heat shock protein expression in Daphnia

Understanding the short- and long-term consequences of climate change is a major challenge in biology. For aquatic organisms, temperature changes and drought can lead to thermal stress and habitat loss, both of which can ultimately lead to higher mutation rates. Here, we examine the effect of high t...

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Autores principales: Scheffer, Henry, Coate, Jeremy E., Ho, Eddie K. H., Schaack, Sarah
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9522699/
https://www.ncbi.nlm.nih.gov/pubmed/36193163
http://dx.doi.org/10.1007/s10682-022-10209-1
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author Scheffer, Henry
Coate, Jeremy E.
Ho, Eddie K. H.
Schaack, Sarah
author_facet Scheffer, Henry
Coate, Jeremy E.
Ho, Eddie K. H.
Schaack, Sarah
author_sort Scheffer, Henry
collection PubMed
description Understanding the short- and long-term consequences of climate change is a major challenge in biology. For aquatic organisms, temperature changes and drought can lead to thermal stress and habitat loss, both of which can ultimately lead to higher mutation rates. Here, we examine the effect of high temperature and mutation accumulation on gene expression at two loci from the heat shock protein (HSP) gene family, HSP60 and HSP90. HSPs have been posited to serve as ‘mutational capacitors’ given their role as molecular chaperones involved in protein folding and degradation, thus buffering against a wide range of cellular stress and destabilization. We assayed changes in HSP expression across 5 genotypes of Daphnia magna, a sentinel species in ecology and environmental biology, with and without acute exposure to thermal stress and accumulated mutations. Across genotypes, HSP expression increased ~ 6× in response to heat and ~ 4× with mutation accumulation, individually. Both factors simultaneously (lineages with high mutation loads exposed to high heat) increased gene expression ~ 23×—much more than that predicted by an additive model. Our results corroborate suggestions that HSPs can buffer against not only the effects of heat, but also mutations—a combination of factors both likely to increase in a warming world. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10682-022-10209-1.
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spelling pubmed-95226992022-10-01 Thermal stress and mutation accumulation increase heat shock protein expression in Daphnia Scheffer, Henry Coate, Jeremy E. Ho, Eddie K. H. Schaack, Sarah Evol Ecol Original Paper Understanding the short- and long-term consequences of climate change is a major challenge in biology. For aquatic organisms, temperature changes and drought can lead to thermal stress and habitat loss, both of which can ultimately lead to higher mutation rates. Here, we examine the effect of high temperature and mutation accumulation on gene expression at two loci from the heat shock protein (HSP) gene family, HSP60 and HSP90. HSPs have been posited to serve as ‘mutational capacitors’ given their role as molecular chaperones involved in protein folding and degradation, thus buffering against a wide range of cellular stress and destabilization. We assayed changes in HSP expression across 5 genotypes of Daphnia magna, a sentinel species in ecology and environmental biology, with and without acute exposure to thermal stress and accumulated mutations. Across genotypes, HSP expression increased ~ 6× in response to heat and ~ 4× with mutation accumulation, individually. Both factors simultaneously (lineages with high mutation loads exposed to high heat) increased gene expression ~ 23×—much more than that predicted by an additive model. Our results corroborate suggestions that HSPs can buffer against not only the effects of heat, but also mutations—a combination of factors both likely to increase in a warming world. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10682-022-10209-1. Springer International Publishing 2022-09-06 2022 /pmc/articles/PMC9522699/ /pubmed/36193163 http://dx.doi.org/10.1007/s10682-022-10209-1 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Original Paper
Scheffer, Henry
Coate, Jeremy E.
Ho, Eddie K. H.
Schaack, Sarah
Thermal stress and mutation accumulation increase heat shock protein expression in Daphnia
title Thermal stress and mutation accumulation increase heat shock protein expression in Daphnia
title_full Thermal stress and mutation accumulation increase heat shock protein expression in Daphnia
title_fullStr Thermal stress and mutation accumulation increase heat shock protein expression in Daphnia
title_full_unstemmed Thermal stress and mutation accumulation increase heat shock protein expression in Daphnia
title_short Thermal stress and mutation accumulation increase heat shock protein expression in Daphnia
title_sort thermal stress and mutation accumulation increase heat shock protein expression in daphnia
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9522699/
https://www.ncbi.nlm.nih.gov/pubmed/36193163
http://dx.doi.org/10.1007/s10682-022-10209-1
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