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Mutation of the toxR or mshA genes from Vibrio coralliilyticus strain OCN014 reduces infection of the coral Acropora cytherea

Blake Ushijima; Patrick Videau; Donna Poscablo; John W. Stengel; Silvia Beurmann; Andrew H. Burger; Greta S. Aeby; Sean M. Callahan
Environmental Microbiology · Vol. 18, Issue 11 · pp. 4055-4067 · 2016

Abstract

Summary Thermal stress increases the incidence of coral disease, which is predicted to become more common with climate change, even on pristine reefs such as those surrounding Palmyra Atoll in the Northern Line Islands that experience minimal anthropogenic stress. Here we describe a strain of Vibrio coralliilyticus , OCN014, which was isolated from Acropora cytherea during an outbreak of Acropora white syndrome (AWS), a tissue loss disease that infected 25% of the A. cytherea population at Palmyra Atoll in 2009. OCN014 recreated signs of disease in experimentally infected corals in a temperature‐dependent manner. Genes in OCN014 with expression levels positively correlated with temperature were identified using a transposon‐mediated genetic screen. Mutant strains harbouring transposon insertions in two such genes, toxR (a toxin regulator) and mshA (the 11th gene of the 16‐gene mannose‐sensitive hemagglutinin (MSHA) type IV pilus operon), had reduced infectivity of A. cytherea . Deletion of toxR and the MSHA operon in a second strain of V. coralliilyticus , OCN008, that induces acute Montipora white syndrome in a temperature‐independent manner had similarly reduced virulence. This work provides a link between temperature‐dependent expression of virulence factors in a pathogen and infection of its coral host.

Bibliographic Information

JournalEnvironmental Microbiology
PublisherWiley
Publication Date2016-11-01
Publication Year2016
Volume18
Issue11
Pages4055-4067
Document TypeJournal Article
Print ISSN1462-2912
eISSN1462-2920
DOI10.1111/1462-2920.13428
SubjectMicrobial Ecology

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NARA Access Coverage1999-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/14622920
Publisher PageOpen Publisher Page
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