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Biological oxygen demand optode analysis of coral reef-associated microbial communities exposed to algal exudates

Algae-derived dissolved organic matter has been hypothesized to induce mortality of reef building corals. One proposed killing mechanism is a zone of hypoxia created by rapidly growing microbes. To investigate this hypothesis, biological oxygen demand (BOD) optodes were used to quantify the change i...

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Autores principales: Gregg, AK, Hatay, M, Haas, AF, Robinett, NL, Barott, K, Vermeij, MJA, Marhaver, KL, Meirelles, P, Thompson, F, Rohwer, F
Formato: Online Artículo Texto
Lenguaje:English
Publicado: PeerJ Inc. 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3719127/
https://www.ncbi.nlm.nih.gov/pubmed/23882444
http://dx.doi.org/10.7717/peerj.107
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author Gregg, AK
Hatay, M
Haas, AF
Robinett, NL
Barott, K
Vermeij, MJA
Marhaver, KL
Meirelles, P
Thompson, F
Rohwer, F
author_facet Gregg, AK
Hatay, M
Haas, AF
Robinett, NL
Barott, K
Vermeij, MJA
Marhaver, KL
Meirelles, P
Thompson, F
Rohwer, F
author_sort Gregg, AK
collection PubMed
description Algae-derived dissolved organic matter has been hypothesized to induce mortality of reef building corals. One proposed killing mechanism is a zone of hypoxia created by rapidly growing microbes. To investigate this hypothesis, biological oxygen demand (BOD) optodes were used to quantify the change in oxygen concentrations of microbial communities following exposure to exudates generated by turf algae and crustose coralline algae (CCA). BOD optodes were embedded with microbial communities cultured from Montastraea annularis and Mussismilia hispida, and respiration was measured during exposure to turf and CCA exudates. The oxygen concentrations along the optodes were visualized with a low-cost Submersible Oxygen Optode Recorder (SOOpR) system. With this system we observed that exposure to exudates derived from turf algae stimulated higher oxygen drawdown by the coral-associated bacteria than CCA exudates or seawater controls. Furthermore, in both turf and CCA exudate treatments, all microbial communities (coral-, algae-associated and pelagic) contributed significantly to the observed oxygen drawdown. This suggests that the driving factor for elevated oxygen consumption rates is the source of exudates rather than the initially introduced microbial community. Our results demonstrate that exudates from turf algae may contribute to hypoxia-induced coral stress in two different coral genera as a result of increased biological oxygen demand of the local microbial community. Additionally, the SOOpR system developed here can be applied to measure the BOD of any culturable microbe or microbial community.
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spelling pubmed-37191272013-07-23 Biological oxygen demand optode analysis of coral reef-associated microbial communities exposed to algal exudates Gregg, AK Hatay, M Haas, AF Robinett, NL Barott, K Vermeij, MJA Marhaver, KL Meirelles, P Thompson, F Rohwer, F PeerJ Ecology Algae-derived dissolved organic matter has been hypothesized to induce mortality of reef building corals. One proposed killing mechanism is a zone of hypoxia created by rapidly growing microbes. To investigate this hypothesis, biological oxygen demand (BOD) optodes were used to quantify the change in oxygen concentrations of microbial communities following exposure to exudates generated by turf algae and crustose coralline algae (CCA). BOD optodes were embedded with microbial communities cultured from Montastraea annularis and Mussismilia hispida, and respiration was measured during exposure to turf and CCA exudates. The oxygen concentrations along the optodes were visualized with a low-cost Submersible Oxygen Optode Recorder (SOOpR) system. With this system we observed that exposure to exudates derived from turf algae stimulated higher oxygen drawdown by the coral-associated bacteria than CCA exudates or seawater controls. Furthermore, in both turf and CCA exudate treatments, all microbial communities (coral-, algae-associated and pelagic) contributed significantly to the observed oxygen drawdown. This suggests that the driving factor for elevated oxygen consumption rates is the source of exudates rather than the initially introduced microbial community. Our results demonstrate that exudates from turf algae may contribute to hypoxia-induced coral stress in two different coral genera as a result of increased biological oxygen demand of the local microbial community. Additionally, the SOOpR system developed here can be applied to measure the BOD of any culturable microbe or microbial community. PeerJ Inc. 2013-07-16 /pmc/articles/PMC3719127/ /pubmed/23882444 http://dx.doi.org/10.7717/peerj.107 Text en © 2013 Gregg et al. http://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Ecology
Gregg, AK
Hatay, M
Haas, AF
Robinett, NL
Barott, K
Vermeij, MJA
Marhaver, KL
Meirelles, P
Thompson, F
Rohwer, F
Biological oxygen demand optode analysis of coral reef-associated microbial communities exposed to algal exudates
title Biological oxygen demand optode analysis of coral reef-associated microbial communities exposed to algal exudates
title_full Biological oxygen demand optode analysis of coral reef-associated microbial communities exposed to algal exudates
title_fullStr Biological oxygen demand optode analysis of coral reef-associated microbial communities exposed to algal exudates
title_full_unstemmed Biological oxygen demand optode analysis of coral reef-associated microbial communities exposed to algal exudates
title_short Biological oxygen demand optode analysis of coral reef-associated microbial communities exposed to algal exudates
title_sort biological oxygen demand optode analysis of coral reef-associated microbial communities exposed to algal exudates
topic Ecology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3719127/
https://www.ncbi.nlm.nih.gov/pubmed/23882444
http://dx.doi.org/10.7717/peerj.107
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