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• W2100085530 endingPage "e107" @default.
• W2100085530 startingPage "e107" @default.
• W2100085530 abstract "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." @default.
• W2100085530 created "2016-06-24" @default.
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• W2100085530 date "2013-07-16" @default.
• W2100085530 modified "2023-09-27" @default.
• W2100085530 title "Biological oxygen demand optode analysis of coral reef-associated microbial communities exposed to algal exudates" @default.
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• W2100085530 doi "https://doi.org/10.7717/peerj.107" @default.
• W2100085530 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3719127" @default.
• W2100085530 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23882444" @default.
• W2100085530 hasPublicationYear "2013" @default.
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