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Biology subjects

Rachel M Wright

Publications and source records attributed to Rachel M Wright.

2 recordsLinked to original sources

Higher stress and immunity responses are associated with higher mortality in reef-building coral exposed to a bacterial challenge

Understanding the drivers of intraspecific variation in susceptibility is essential to manage increasingly frequent coral disease outbreaks. We challenged replicate fragments of eight Acropora millepora genotypes with Vibrio spp. to quantify variation in lesion development and to identify host and coral-associated microbial community properties associated with resistance. While Vibrio spp. remained relatively rare in the microbiome of challenged corals, other stress-associated microbial taxa significantly increased in abundance. Contrary to expectations, higher constitutive immunity and more active immune responses did not confer higher resistance to bacterial challenge. Furthermore, more pronounced gene expression responses to bacterial challenge were associated with higher rather than lower mortality. A newly developed gene expression assay based on two genes related to inflammation and immune responses, deleted in malignant brain tumors 1 and a matrix metalloproteinase, predicted mortality under Vibrio treatment both in the initial experiment and in a validation experiment involving another 20 A. millepora genotypes. Instead of mounting more robust responses, resistant corals were largely unaffected by the bacterial challenge and maintained gene expression signatures of healthier condition, including elevated fluorescent proteins and ribosomal biosynthesis along with diminished ubiquitination. Overall, our results support the view that coral disease and mortality is commonly due to opportunistic pathogens exploiting physiologically compromised hosts rather than specific infections, and show, contrary to the prevailing wisdom, that greater immune responses do not necessarily translate into greater disease resistance.

Ecology

Gene expression associated with white syndromes in a reef building coral, Acropora hyacinthus.

BackgroundCorals are capable of launching diverse immune defenses at the site of direct contact with pathogens, but the molecular mechanisms of this activity and the colony-wide effects of such stressors remain poorly understood. Here we compared gene expression profiles in eight healthy Acropora hyacinthus colonies against eight colonies exhibiting tissue loss commonly associated with white syndromes, all collected from a natural reef environment near Palau. Two types of tissues were sampled from diseased corals: visibly affected and apparently healthy.\n\nResultsTag-based RNA-Seq followed by weighted gene co-expression network analysis identified groups of co-regulated differentially expressed genes between all health states (disease lesion, apparently healthy tissues of diseased colonies, and fully healthy). Differences between healthy and diseased tissues indicate activation of several innate immunity and tissue repair pathways accompanied by reduced calcification and the switch towards metabolic reliance on stored lipids. Unaffected parts of diseased colonies, although displaying a trend towards these changes, were not significantly different from fully healthy samples. Still, network analysis identified a group of genes, suggestive of altered immunity state, that were specifically up-regulated in unaffected parts of diseased colonies.\n\nConclusionsSimilarity of fully healthy samples to apparently healthy parts of diseased colonies indicates that systemic effects of white syndromes on A. hyacinthus are weak, which implies that the coral colony is largely able to sustain its physiological performance despite disease. The genes specifically up-regulated in unaffected parts of diseased colonies, instead of being the consequence of disease, might be related to the originally higher susceptibility of these colonies to naturally occurring white syndromes.

Genomics