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The response of a boreal deep-sea sponge holobiont to acute thermal stress
Effects of elevated seawater temperatures on deep-water benthos has been poorly studied, despite reports of increased seawater temperature (up to 4 °C over 24 hrs) coinciding with mass mortality events of the sponge Geodia barretti at Tisler Reef, Norway. While the mechanisms driving these mortality...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5440399/ https://www.ncbi.nlm.nih.gov/pubmed/28533520 http://dx.doi.org/10.1038/s41598-017-01091-x |
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author | Strand, R. Whalan, S. Webster, N. S. Kutti, T. Fang, J. K. H. Luter, H. M. Bannister, R. J. |
author_facet | Strand, R. Whalan, S. Webster, N. S. Kutti, T. Fang, J. K. H. Luter, H. M. Bannister, R. J. |
author_sort | Strand, R. |
collection | PubMed |
description | Effects of elevated seawater temperatures on deep-water benthos has been poorly studied, despite reports of increased seawater temperature (up to 4 °C over 24 hrs) coinciding with mass mortality events of the sponge Geodia barretti at Tisler Reef, Norway. While the mechanisms driving these mortality events are unclear, manipulative laboratory experiments were conducted to quantify the effects of elevated temperature (up to 5 °C, above ambient levels) on the ecophysiology (respiration rate, nutrient uptake, cellular integrity and sponge microbiome) of G. barretti. No visible signs of stress (tissue necrosis or discolouration) were evident across experimental treatments; however, significant interactive effects of time and treatment on respiration, nutrient production and cellular stress were detected. Respiration rates and nitrogen effluxes doubled in responses to elevated temperatures (11 °C & 12 °C) compared to control temperatures (7 °C). Cellular stress, as measured through lysosomal destabilisation, was 2–5 times higher at elevated temperatures than for control temperatures. However, the microbiome of G. barretti remained stable throughout the experiment, irrespective of temperature treatment. Mortality was not evident and respiration rates returned to pre-experimental levels during recovery. These results suggest other environmental processes, either alone or in combination with elevated temperature, contributed to the mortality of G. barretti at Tisler reef. |
format | Online Article Text |
id | pubmed-5440399 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-54403992017-05-25 The response of a boreal deep-sea sponge holobiont to acute thermal stress Strand, R. Whalan, S. Webster, N. S. Kutti, T. Fang, J. K. H. Luter, H. M. Bannister, R. J. Sci Rep Article Effects of elevated seawater temperatures on deep-water benthos has been poorly studied, despite reports of increased seawater temperature (up to 4 °C over 24 hrs) coinciding with mass mortality events of the sponge Geodia barretti at Tisler Reef, Norway. While the mechanisms driving these mortality events are unclear, manipulative laboratory experiments were conducted to quantify the effects of elevated temperature (up to 5 °C, above ambient levels) on the ecophysiology (respiration rate, nutrient uptake, cellular integrity and sponge microbiome) of G. barretti. No visible signs of stress (tissue necrosis or discolouration) were evident across experimental treatments; however, significant interactive effects of time and treatment on respiration, nutrient production and cellular stress were detected. Respiration rates and nitrogen effluxes doubled in responses to elevated temperatures (11 °C & 12 °C) compared to control temperatures (7 °C). Cellular stress, as measured through lysosomal destabilisation, was 2–5 times higher at elevated temperatures than for control temperatures. However, the microbiome of G. barretti remained stable throughout the experiment, irrespective of temperature treatment. Mortality was not evident and respiration rates returned to pre-experimental levels during recovery. These results suggest other environmental processes, either alone or in combination with elevated temperature, contributed to the mortality of G. barretti at Tisler reef. Nature Publishing Group UK 2017-05-22 /pmc/articles/PMC5440399/ /pubmed/28533520 http://dx.doi.org/10.1038/s41598-017-01091-x Text en © The Author(s) 2017 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 Strand, R. Whalan, S. Webster, N. S. Kutti, T. Fang, J. K. H. Luter, H. M. Bannister, R. J. The response of a boreal deep-sea sponge holobiont to acute thermal stress |
title | The response of a boreal deep-sea sponge holobiont to acute thermal stress |
title_full | The response of a boreal deep-sea sponge holobiont to acute thermal stress |
title_fullStr | The response of a boreal deep-sea sponge holobiont to acute thermal stress |
title_full_unstemmed | The response of a boreal deep-sea sponge holobiont to acute thermal stress |
title_short | The response of a boreal deep-sea sponge holobiont to acute thermal stress |
title_sort | response of a boreal deep-sea sponge holobiont to acute thermal stress |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5440399/ https://www.ncbi.nlm.nih.gov/pubmed/28533520 http://dx.doi.org/10.1038/s41598-017-01091-x |
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