Dataset Information

Pseudoalteromonas piratica strain OCN003 is a coral pathogen that causes a switch from chronic to acute Montipora white syndrome in Montipora capitata.

ABSTRACT: Reports of mass coral mortality from disease have increased over the last two decades. Montipora white syndrome (MWS) is a tissue loss disease that has negatively impacted populations of the coral Montipora capitata in K?ne'ohe Bay, Hawai'i. Two types of MWS have been documented; a progressive disease termed chronic MWS (cMWS), that can be caused by Vibrio owensii strain OCN002, and a comparatively faster disease termed acute MWS (aMWS), that can be caused by Vibrio coralliilyticus strain OCN008. M. capitata colonies exhibiting cMWS can spontaneously switch to aMWS in the field. In this study, a novel Pseudoalteromonas species, P. piratica strain OCN003, fulfilled Koch's postulates of disease causation as another etiological agent of aMWS. Additionally, OCN003 induced a switch from cMWS to aMWS on M. capitata in laboratory infection trials. A comparison of OCN003 and Vibrio coralliilyticus strain OCN008, showed that OCN003 was more effective at inducing the cMWS to aMWS switch in M. capitata than OCN008. This study is the first to demonstrate that similar disease signs on one coral species (aMWS on M. capitata) can be caused by multiple pathogens, and describes the first Pseudoalteromonas species that infects coral.

SUBMITTER: Beurmann S

PROVIDER: S-EPMC5690655 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Pseudoalteromonas piratica strain OCN003 is a coral pathogen that causes a switch from chronic to acute Montipora white syndrome in Montipora capitata.

Beurmann Silvia S Ushijima Blake B Videau Patrick P Svoboda Christina Marie CM Smith Ashley Marie AM Rivers Orion Silverstar OS Aeby Greta Smith GS Callahan Sean Michael SM

PloS one 20171116 11

Reports of mass coral mortality from disease have increased over the last two decades. Montipora white syndrome (MWS) is a tissue loss disease that has negatively impacted populations of the coral Montipora capitata in Kāne'ohe Bay, Hawai'i. Two types of MWS have been documented; a progressive disease termed chronic MWS (cMWS), that can be caused by Vibrio owensii strain OCN002, and a comparatively faster disease termed acute MWS (aMWS), that can be caused by Vibrio coralliilyticus strain OCN008 ...[more]

PMID: 29145488

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Project description:Background Corals, which form the foundation of biodiverse reef ecosystems, are under threat from warming oceans. Reefs provide essential ecological services, including food, income from tourism, nutrient cycling, waste removal, and the absorption of wave energy to mitigate erosion. Here, we studied the coral thermal stress response using network methods to analyze transcriptomic and polar metabolomic data generated from the Hawaiian rice coral Montipora capitata. Coral nubbins were exposed to ambient or thermal stress conditions over a 5-week period, coinciding with a mass spawning event of this species. The major goal of our study was to expand the inventory of thermal stress-related genes and metabolites present in M. capitata and to study gene-metabolite interactions. These interactions provide the foundation for functional or genetic analysis of key coral genes as well as provide potentially diagnostic markers of pre-bleaching stress. A secondary goal of our study was to analyze the accumulation of sex hormones prior to and during mass spawning to understand how thermal stress may impact reproductive success in M. capitata. Methods M. capitata was exposed to thermal stress during its spawning cycle over the course of 5 weeks, during which time transcriptomic and polar metabolomic data were collected. We analyzed these data streams individually, and then integrated both data sets using MAGI (Metabolite Annotation and Gene Integration) to investigate molecular transitions and biochemical reactions. Results Our results reveal the complexity of the thermal stress phenome in M. capitata, which includes many genes involved in redox regulation, biomineralization, and reproduction. The size and number of modules in the gene co-expression networks expanded from the initial stress response to the onset of bleaching. The later stages involved the suppression of metabolite transport by the coral host, including a variety of sodium-coupled transporters and a putative ammonium transporter, possibly as a response to reduction in algal productivity. The gene-metabolite integration data suggest that thermal treatment results in the activation of animal redox stress pathways involved in quenching molecular oxygen to prevent an overabundance of reactive oxygen species. Lastly, evidence that thermal stress affects reproductive activity was provided by the downregulation of CYP-like genes and the irregular production of sex hormones during the mass spawning cycle. Overall, redox regulation and metabolite transport are key components of the coral animal thermal stress phenome. Mass spawning was highly attenuated under thermal stress, suggesting that global climate change may negatively impact reproductive behavior in this species.

Project description:Scleractinian corals are a vital component of coral reef ecosystems, and of significant cultural and economic value worldwide. As anthropogenic and natural stressors are contributing to a global decline of coral reefs, understanding coral health is critical to help preserve these ecosystems. Growth anomaly (GA) is a coral disease that has significant negative impacts on coral biology, yet our understanding of its etiology and pathology is lacking. In this study we used RNA-seq along with de novo metatranscriptome assembly and homology assignment to identify coral genes that are expressed in three distinct coral tissue types: tissue from healthy corals ("healthy"), GA lesion tissue from diseased corals ("GA-affected") and apparently healthy tissue from diseased corals ("GA-unaffected"). We conducted pairwise comparisons of gene expression among these three tissue types to identify genes and pathways that help us to unravel the molecular pathology of this coral disease.The quality-filtered de novo-assembled metatranscriptome contained 76,063 genes, of which 13,643 were identified as putative coral genes. Overall gene expression profiles of coral genes revealed high similarity between healthy tissue samples, in contrast to high variance among diseased samples. This indicates GA has a variety of genetic effects at the colony level, including on seemingly healthy (GA-unaffected) tissue. A total of 105 unique coral genes were found differentially expressed among tissue types. Pairwise comparisons revealed the greatest number of differentially expressed genes between healthy and GA-affected tissue (93 genes), followed by healthy and GA-unaffected tissue (33 genes), and GA-affected and -unaffected tissue (7 genes). The putative function of these genes suggests GA is associated with changes in the activity of genes involved in developmental processes and activation of the immune system.This is one of the first transcriptome-level studies to investigate coral GA, and the first metatranscriptome assembly for the M. capitata holobiont. The gene expression data, metatranscriptome assembly and methodology developed through this study represent a significant addition to the molecular information available to further our understanding of this coral disease.

Dataset Information

Pseudoalteromonas piratica strain OCN003 is a coral pathogen that causes a switch from chronic to acute Montipora white syndrome in Montipora capitata.

Publications

Pseudoalteromonas piratica strain OCN003 is a coral pathogen that causes a switch from chronic to acute Montipora white syndrome in Montipora capitata.

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