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Anthropogenic stressors impact fish sensory development and survival via thyroid disruption
Larval metamorphosis and recruitment represent critical life-history transitions for most teleost fishes. While the detrimental effects of anthropogenic stressors on the behavior and survival of recruiting fishes are well-documented, the physiological mechanisms that underpin these patterns remain u...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7367887/ https://www.ncbi.nlm.nih.gov/pubmed/32681015 http://dx.doi.org/10.1038/s41467-020-17450-8 |
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author | Besson, Marc Feeney, William E. Moniz, Isadora François, Loïc Brooker, Rohan M. Holzer, Guillaume Metian, Marc Roux, Natacha Laudet, Vincent Lecchini, David |
author_facet | Besson, Marc Feeney, William E. Moniz, Isadora François, Loïc Brooker, Rohan M. Holzer, Guillaume Metian, Marc Roux, Natacha Laudet, Vincent Lecchini, David |
author_sort | Besson, Marc |
collection | PubMed |
description | Larval metamorphosis and recruitment represent critical life-history transitions for most teleost fishes. While the detrimental effects of anthropogenic stressors on the behavior and survival of recruiting fishes are well-documented, the physiological mechanisms that underpin these patterns remain unclear. Here, we use pharmacological treatments to highlight the role that thyroid hormones (TH) play in sensory development and determining anti-predator responses in metamorphosing convict surgeonfish, Acanthurus triostegus. We then show that high doses of a physical stressor (increased temperature of +3 °C) and a chemical stressor (the pesticide chlorpyrifos at 30 µg L(−1)) induced similar defects by decreasing fish TH levels and affecting their sensory development. Stressor-exposed fish experienced higher predation; however, their ability to avoid predation improved when they received supplemental TH. Our results highlight that two different anthropogenic stressors can affect critical developmental and ecological transitions via the same physiological pathway. This finding provides a unifying mechanism to explain past results and underlines the profound threat anthropogenic stressors pose to fish communities. |
format | Online Article Text |
id | pubmed-7367887 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-73678872020-07-21 Anthropogenic stressors impact fish sensory development and survival via thyroid disruption Besson, Marc Feeney, William E. Moniz, Isadora François, Loïc Brooker, Rohan M. Holzer, Guillaume Metian, Marc Roux, Natacha Laudet, Vincent Lecchini, David Nat Commun Article Larval metamorphosis and recruitment represent critical life-history transitions for most teleost fishes. While the detrimental effects of anthropogenic stressors on the behavior and survival of recruiting fishes are well-documented, the physiological mechanisms that underpin these patterns remain unclear. Here, we use pharmacological treatments to highlight the role that thyroid hormones (TH) play in sensory development and determining anti-predator responses in metamorphosing convict surgeonfish, Acanthurus triostegus. We then show that high doses of a physical stressor (increased temperature of +3 °C) and a chemical stressor (the pesticide chlorpyrifos at 30 µg L(−1)) induced similar defects by decreasing fish TH levels and affecting their sensory development. Stressor-exposed fish experienced higher predation; however, their ability to avoid predation improved when they received supplemental TH. Our results highlight that two different anthropogenic stressors can affect critical developmental and ecological transitions via the same physiological pathway. This finding provides a unifying mechanism to explain past results and underlines the profound threat anthropogenic stressors pose to fish communities. Nature Publishing Group UK 2020-07-17 /pmc/articles/PMC7367887/ /pubmed/32681015 http://dx.doi.org/10.1038/s41467-020-17450-8 Text en © The Author(s) 2020 Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Besson, Marc Feeney, William E. Moniz, Isadora François, Loïc Brooker, Rohan M. Holzer, Guillaume Metian, Marc Roux, Natacha Laudet, Vincent Lecchini, David Anthropogenic stressors impact fish sensory development and survival via thyroid disruption |
title | Anthropogenic stressors impact fish sensory development and survival via thyroid disruption |
title_full | Anthropogenic stressors impact fish sensory development and survival via thyroid disruption |
title_fullStr | Anthropogenic stressors impact fish sensory development and survival via thyroid disruption |
title_full_unstemmed | Anthropogenic stressors impact fish sensory development and survival via thyroid disruption |
title_short | Anthropogenic stressors impact fish sensory development and survival via thyroid disruption |
title_sort | anthropogenic stressors impact fish sensory development and survival via thyroid disruption |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7367887/ https://www.ncbi.nlm.nih.gov/pubmed/32681015 http://dx.doi.org/10.1038/s41467-020-17450-8 |
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