Quorum Sensing in the Hawaiian Coral Pathogen Vibrio coralliilyticus strain OCN008.

dc.contributor.author Burger, Andrew H.
dc.contributor.department Microbiology
dc.date.accessioned 2019-05-28T20:15:07Z
dc.date.available 2019-05-28T20:15:07Z
dc.date.issued 2017-08
dc.identifier.uri http://hdl.handle.net/10125/62546
dc.subject Vibrio coralliilyticus
dc.subject quorum sensing
dc.subject coral disease
dc.title Quorum Sensing in the Hawaiian Coral Pathogen Vibrio coralliilyticus strain OCN008.
dc.type Thesis
dcterms.abstract Coral disease represents a serious threat to reefs worldwide. Reef ecosystems have been reshaped by coral disease in the Caribbean, Florida Keys, and the Great Barrier Reef. Reefs represent millions of dollars in economic value as well as contribute heavily to marine primary production, thus efforts to minimize such damage have become crucial. Coral disease in Hawaiʻi has presented less of a problem when compared to the Caribbean, but emerging diseases over the past decade have brought the potential for similar destruction. One disease of concern in Kāneʻohe Bay, Oahu, is Acute Montipora White Syndrome (aMWS), a rapidly progressing tissue-loss disease affecting the reef-building coral Montipora capitata. Early efforts studying this disease identified Vibrio coralliilyticus strain OCN008 as an etiological agent of aMWS. Interestingly, OCN008 produces and utilizes the antibiotic andrimid as a novel virulence factor. This discovery represented one of only a handful (<5) of known virulence factors in the field of coral disease, and potentially provides a point at which to begin investigations into preventative and/or curative strategies. This work describes the quorum sensing (cell-density dependent bacterial communication/behavior) mechanics of strain OCN008. The main objectives were the identification and characterization of putative quorum sensing circuits and the role they play in the infection of M. capitata. Despite possessing homologs of four known Vibrio quorum sensing pathways, OCN008 requires only one, the LuxPQ/S pathway (AI-2), to activate the high cell density response. Quorum sensing also contributes to the virulence of OCN008 at both low and high cell densities. Since the novel virulence factor andrimid was shown here to be under regulation of AI-2 mediated quorum sensing, a scenario is presented in which OCN008 can initiate andrimid production in response to a quorum of AI-2 producing bacteria, regardless of taxonomy. Interestingly, the two most severe outbreaks of aMWS were recorded following periods of heavy rain, events known to cause increased bacterial abundance and perturbations in coastal microbial communities. Shifts in coral microbiota have been linked to increased incidents of coral disease. This work offers one potential mechanism behind this phenomenon. In addition, this work offers the first direct evidence that quorum sensing is involved in coral disease.
dcterms.description Ph.D. Thesis. University of Hawaiʻi at Mānoa 2017.
dcterms.language eng
dcterms.publisher University of Hawaiʻi at Mānoa
dcterms.rights All UHM dissertations and theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission from the copyright owner.
dcterms.type Text
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