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Evolution to environmental contamination ablates the circadian clock of an aquatic sentinel species
Environmental contamination is a common cause of rapid evolution. Recent work has shown that Daphnia pulex, an important freshwater species, can rapidly evolve increased tolerance to a common contaminant, sodium chloride (NaCl) road salt. While such rapid evolution can benefit organisms, allowing th...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5723614/ https://www.ncbi.nlm.nih.gov/pubmed/29238559 http://dx.doi.org/10.1002/ece3.3490 |
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author | Coldsnow, Kayla D. Relyea, Rick A. Hurley, Jennifer M. |
author_facet | Coldsnow, Kayla D. Relyea, Rick A. Hurley, Jennifer M. |
author_sort | Coldsnow, Kayla D. |
collection | PubMed |
description | Environmental contamination is a common cause of rapid evolution. Recent work has shown that Daphnia pulex, an important freshwater species, can rapidly evolve increased tolerance to a common contaminant, sodium chloride (NaCl) road salt. While such rapid evolution can benefit organisms, allowing them to adapt to new environmental conditions, it can also be associated with unforeseen tradeoffs. Given that exposure to environmental contaminants can cause circadian disruption, we investigated whether the circadian clock was affected by evolving a tolerance to high levels of road salt. By tracking the oscillations of a putative clock gene, period, we demonstrated that D. pulex express per mRNA with approximately 20‐hr oscillations under control conditions. This putative circadian rhythm was ablated in response to high levels of salinity; populations adapted to high NaCl concentrations exhibited an ablation of period oscillation. Moreover, we showed that while gene expression is increased in several other genes, including clock, actin, and Na (+) /K (+) ‐ATPase, upon the adaptation to high levels of salinity, per expression is unique among the genes we tracked in that it is the only gene repressed in response to salt adaptation. These results suggest that rapid evolution of salt tolerance occurs with the tradeoff of suppressed circadian function. The resultant circadian disruption may have profound consequences to individuals, populations, and aquatic food webs by affecting species interactions. In addition, our research suggests that circadian clocks may also be disrupted by the adaptation to other environmental contaminants. |
format | Online Article Text |
id | pubmed-5723614 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-57236142017-12-13 Evolution to environmental contamination ablates the circadian clock of an aquatic sentinel species Coldsnow, Kayla D. Relyea, Rick A. Hurley, Jennifer M. Ecol Evol Original Research Environmental contamination is a common cause of rapid evolution. Recent work has shown that Daphnia pulex, an important freshwater species, can rapidly evolve increased tolerance to a common contaminant, sodium chloride (NaCl) road salt. While such rapid evolution can benefit organisms, allowing them to adapt to new environmental conditions, it can also be associated with unforeseen tradeoffs. Given that exposure to environmental contaminants can cause circadian disruption, we investigated whether the circadian clock was affected by evolving a tolerance to high levels of road salt. By tracking the oscillations of a putative clock gene, period, we demonstrated that D. pulex express per mRNA with approximately 20‐hr oscillations under control conditions. This putative circadian rhythm was ablated in response to high levels of salinity; populations adapted to high NaCl concentrations exhibited an ablation of period oscillation. Moreover, we showed that while gene expression is increased in several other genes, including clock, actin, and Na (+) /K (+) ‐ATPase, upon the adaptation to high levels of salinity, per expression is unique among the genes we tracked in that it is the only gene repressed in response to salt adaptation. These results suggest that rapid evolution of salt tolerance occurs with the tradeoff of suppressed circadian function. The resultant circadian disruption may have profound consequences to individuals, populations, and aquatic food webs by affecting species interactions. In addition, our research suggests that circadian clocks may also be disrupted by the adaptation to other environmental contaminants. John Wiley and Sons Inc. 2017-10-28 /pmc/articles/PMC5723614/ /pubmed/29238559 http://dx.doi.org/10.1002/ece3.3490 Text en © 2017 The Authors. Ecology and Evolution published by John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Coldsnow, Kayla D. Relyea, Rick A. Hurley, Jennifer M. Evolution to environmental contamination ablates the circadian clock of an aquatic sentinel species |
title | Evolution to environmental contamination ablates the circadian clock of an aquatic sentinel species |
title_full | Evolution to environmental contamination ablates the circadian clock of an aquatic sentinel species |
title_fullStr | Evolution to environmental contamination ablates the circadian clock of an aquatic sentinel species |
title_full_unstemmed | Evolution to environmental contamination ablates the circadian clock of an aquatic sentinel species |
title_short | Evolution to environmental contamination ablates the circadian clock of an aquatic sentinel species |
title_sort | evolution to environmental contamination ablates the circadian clock of an aquatic sentinel species |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5723614/ https://www.ncbi.nlm.nih.gov/pubmed/29238559 http://dx.doi.org/10.1002/ece3.3490 |
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