Abstract
Disease causes significant coral mortality worldwide; however, factors responsible for intraspecific variation in disease resistance remain unclear. We exposed fragments of eight Acropora millepora colonies (genotypes) to putatively pathogenic bacteria (Vibrio spp.). Genotypes varied from zero to >90% mortality, with bacterial challenge increasing average mortality rates 4–6 fold and shifting the microbiome in favor of stress-associated taxa. Constitutive immunity and subsequent immune and transcriptomic responses to the challenge were more prominent in high-mortality individuals, whereas low-mortality corals remained largely unaffected and maintained expression signatures of a healthier condition (i.e., did not launch a large stress response). Our results suggest that lesions appeared due to changes in the coral pathobiome (multiple bacterial species associated with disease) and general health deterioration after the biotic disturbance, rather than the direct activity of any specific pathogen. If diseases in nature arise because of weaknesses in holobiont physiology, instead of the virulence of any single etiological agent, environmental stressors compromising coral condition might play a larger role in disease outbreaks than is currently thought. To facilitate the diagnosis of compromised individuals, we developed and independently cross-validated a biomarker assay to predict mortality based on genes whose expression in asymptomatic individuals coincides with mortality rates.
Highlights
Global declines in coral cover are compounded by a variety of diseases[1, 2], many of which are ambiguously defined by macroscopic characterizations of lesions[1,2,3]
No lesions formed under control conditions in any genotype, whereas some fragments died after abrasion (Fig. 1A) and many more died under bacterial or combined treatment (Fig. 1B)
The increased mortality was similar between challenge agents (V. diazotrophicus: 5.7-fold; V. owensii: 3.7-fold), and there was no significant difference in time-dependent mortality between the two bacterial species (Supplementary Fig. S2; p = 0.108)
Summary
Global declines in coral cover are compounded by a variety of diseases[1, 2], many of which are ambiguously defined by macroscopic characterizations of lesions[1,2,3]. Several bacterial species from the genus Vibrio have been implicated as etiological agents of some coral diseases[4,5,6], but these bacteria may act merely as opportunistic pathogens exploiting compromised hosts[7]. We comprehensively examine coral host immune activity, genome-wide gene expression, Symbiodinium profiles, and coral-associated microbial communities in a bacterial challenge experiment to understand the physiological and molecular features underpinning intraspecific variation in mortality rate. Fragments of eight colonies of Acropora millepora from two locations on the Great Barrier Reef (GBR) were individually challenged in a full-factorial design with bacteria (Vibrio owensii and V. diazotrophicus) and mechanical abrasion (n = 3 per experimental group, Fig. S1) These fragments were monitored over a week of lesion development and progression. Post-challenge, yet asymptomatic, samples demonstrated genotype-specific gene expression responses to the bacterial challenges
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