Coral diseases were unknown in the scientific community fifty years ago. Since the discovery of a coral disease in 1965, there has been an exponential increase in the number of known coral diseases, as the abundance, prevalence, distribution, and number of host species affected has also significantly increased. Coral diseases are recognized as contributing significantly to the dramatic losses of coral cover on a global basis, particularly in the Caribbean. The apparent sudden emergence of coral diseases suggests that they may be a symptom of an overall trend associated with changing environmental conditions. However, not much evidence has been gathered to address this question. The following studies were designed to build a comprehensive argument to support this hypothesis for one important coral disease – black band disease (BBD). A meta-analysis of clone libraries identifying the microbial communities associated with BBD reveal important information including that a single cyanobacterial operational taxonomic unit (OTU) was by far the most prevalent OTU in diseased samples, and that the alphaproteobacteria, which include some of the most common bacteria in marine waters, were the most diversely represented. The analysis also showed that samples exhibited regional similarities. An fine and ultrastructural characterization of the disease revealed that the cyanobacteria are prolific borers through the coral skeleton, and that the cyanobacteria penetrate coral tissue, leading to their presence ahead of the main migrating disease band. It was further found that apparently healthy corals exposed to toxins found in BBD, exhibited similar tissue degradation to those infected with BBD. Comparing the disease progression to biofilm formation, it was determined that scouting cyanobacteria may contribute to the migration of the disease through progressive biofilm development over intact coral tissue. Together, these studies provide significant evidence for the hypothesis that BBD is an opportunistic disease, caused by common environmental bacteria, facilitated by the changing environmental conditions associated with climate change.

Coral reef ecosystems are under increasing threat from ocean warming and deoxygenation. Mass coral bleaching events in recent years have been linked to marine heatwaves but reporting of hypoxia-induced bleaching has also been increasing. Oxygen availability in coral reefs is driven by community metabolism and they experience a dynamic range of oxygen concentrations throughout diel cycles, hyperoxia during the day and hypoxia during the night. It has been suggested that the highest oxygen concentrations coincide with the hottest part of the day and this may protect marine taxa from high temperatures. We evaluated experimentally whether excess oxygen availability would increase the thermal threshold of the branching coral Stylophora pistillata, from the Southern Red Sea. We did this by exposing coral fragments of this species to varying dissolved oxygen concentrations (hypoxia, normoxia and hyperoxia) and a short-term temperature ramping regime (1˚C h-1). Hyperoxia did extend the thermal tolerance of S. pistillata fragments, with an LT50 of 39.1˚C as opposed to 39.0˚C for the normoxic treatment and 38.7˚C for the hypoxic treatment. Hyperoxia also increased respiration and gross photosynthesis and had a negative effect on photochemical efficiency at high temperatures. Net photosynthesis, P:R ratio and symbiont density were not significantly affected by oxygen concentration. Corals in this experiment displayed exceedingly high thermal thresholds, which were at least 2˚C higher than previously reported for the same species in the Central Red Sea. The corals used in the experiment had previously survived mass bleaching events in 2015 and hence we may have selected for individuals adapted to thermal stress. This is the first study to investigate the role of oxygen in the thermal tolerance of hermatypic corals and the first assessment of thermal thresholds from corals in the Southern Red Sea, where previously thermal thresholds have been based on a 1-2˚C increase in maximum mean monthly temperatures and visual bleaching observations. This highlights the need for increased experimental assessments of thermal thresholds in the Southern regions of the Red Sea and the important role of oxygen in moderating thermal stress.

Scleractinian corals represent the foundation species of one of the most diverse and productive ecosystem on earth, coral reefs. Corals not only constitute the trophic basis of these ecosystems, but also provide essential habitats and shelter for a wide variety of marine species, many of which are commercially relevant. They also provide other important ecosystem services such as food provision, shoreline protection and opportunities for ecotourism. Despite the ecological importance of corals, very little is known about how their soft-bodied ancestor evolved the ability to form a calcified skeleton and became the ecosystem builders they are today. Corallimorpharia are closely related to reef-building corals but lack the ability to form calcified skeletons. Here we assembled and annotated two draft genomes of the corallimorpharians, Amplexidiscus fenestrafer and Discosoma sp., and further provided an online interface to facilitate the use of these resources. The two genomes can not only inform on the current evolutionary gap in genomic resources for the subclass of Hexacorallia but also provide important resources for comparative genomic studies aiming at understanding the evolution of coral specific traits. Our broad phylogenomic approach using whole genome data, including phylogenetic analyses of nuclear encoding genes as well as genome-wide presence/absence information and synteny conservation from six hexacorallian species, provides robust evidence that corallimorpharians are a monophyletic sister group of scleractinians, therefore rejecting the “naked coral” hypothesis. Being the closest non-calcifying relative of scleractinian corals, corallimorpharians appear to be the best candidates to understand the evolutionary origin of coral calcification. Molecular divergence analysis of scleractinian coral and Corallimorpharia genes suggests that the soft-bodied ancestor of corals evolved the ability to calcify within approximately 80 million years after the divergence of these two orders. To uncover the molecular basis of coral skeletal formation and growth, we integrate genomic and transcriptomic data as well as skeletal proteomic data, and show that gene and domain duplications have been the main evolutionary mechanisms underlying the evolution of calcification in scleractinian corals.

Parrotfishes (Scarinae) are dominant Caribbean herbivores that play an important role in reducing coral-algae competition by grazing algae; yet some species are also occasional coral predators (corallivores) and thereby can have direct negative impacts on coral growth and survivorship. There is concern that parrotfish corallivory may contribute to substantial long-term declines in targeted coral species, particularly in areas with a high biomass of parrotfishes and low cover of corals. However, the capacity of target coral species to heal from parrotfish predation and the ecological drivers of corallivory are poorly understood. In Chapter 1, we examined the patterns of coral healing from parrotfish predation scars on Orbicella annularis – an ecologically important framework building coral that is one of the most intensely grazed Caribbean coral species and an endangered species. While some researchers have suggested that parrotfishes may have significant long-term impacts on heavily targeted species such as O. annularis, the patterns of coral recovery from parrotfish predation scars remain poorly understood. To address this knowledge gap, we tracked the fate of parrotfish bite scars on O. annularis colonies across two Caribbean islands for up to two months. We evaluated differences in coral healing between islands in response to a number of variables including the initial scar surface area, scar abundance per coral colony, colony surface area, and water depth. We used these data to develop a predictive model of O. annularis tissue loss from recent parrotfish bite scars. We then applied this model to surveys of the distribution of bite scars at a point in time to estimate long-term tissue loss of O. annularis colonies from a standing stock of bite scars. Our findings suggest that the initial scar surface area is one of the most important predictors of coral tissue loss. The data also indicate that there are thresholds in patterns of coral tissue regeneration: we observed that small scars (≤1.25 cm2) often fully heal, while larger scars (≥8.2 cm2) had minimal tissue regeneration. The vast majority of observed scars (~87%) were 1.25 cm2 or less and our model predicted that O. annularis colonies would regenerate nearly all the corresponding scar area. In contrast, while scars greater than or equal to than 8.2 cm2 were infrequent (~6% of all observed scars), our model predicted that these larger scars would account for over 96% of the total tissue loss for grazed colonies. Overall, our results suggest that the immediate negative impacts of parrotfish predation on coral tissue loss appear to be driven primarily by a few exceptionally large bite scars. While further work is needed to understand the long-term impacts of corallivory and quantify the net impacts of parrotfish herbivory and corallivory on Caribbean coral reefs, this study is an important step in addressing factors that impact the recovery of a heavily targeted and ecologically important Caribbean coral from parrotfish predation. In Chapter 2, we examined the ecological drivers of corallivory across all coral taxa and across three regions of the Greater Caribbean – the Florida Keys, St. Croix, and Bonaire. To do so, we observed how parrotfish grazing intensity varied using both size and abundance-based metrics across multiple spatial scales. At the reef community and regional scale, we found no effect of the biomass of corallivorous parrotfishes or the percent cover of target coral species on the intensity of parrotfish corallivory. However, at the scale of individual coral colonies, we found that coral taxa and colony size were important predictors of corallivory intensity, and that predation intensity increased as colony size increased. Our findings suggest that previous assertions that conservation of corallivorous parrotfishes may have net negative impacts on coral communities, particularly as live coral cover declines, are not supported at the reef-scale. Instead, our research suggests that colony-level traits such as coral taxa and colony size may be stronger drivers of predation intensity. Additionally, our research suggests that parrotfishes do not heavily graze upon the majority of coral species, but have a higher level of grazing intensity on three taxa, Orbicella annularis, Porites astreoides and other Porites spp. across multiple regions of the Caribbean. Therefore, the direct consequences of parrotfish corallivory for coral tissue loss are likely low for the majority of coral species, but further research is needed to better understand the ultimate causes of selective predation and the long-term consequences of corallivory for heavily targeted coral taxa.

Coral reefs are among the most biodiverse ecosystems in the world, being essential for marine life. The engineers of these ecosystems, reef-building corals, live in association with a great diversity of microorganisms, which can affect their host’s health in beneficial or detrimental manners. Corals are currently threatened by climate change and other environmental stressors, that lead to the phenomenon of coral bleaching, in which these animals lose their endosymbiotic algae. Even though the stressors that cause coral bleaching are known, the exact cellular and molecular mechanisms that provoke this process are still undiscovered. The lack of information regarding micro-scale processes that happen in unhealthy corals could be resolved with more efforts in developing micro-scale studying models. The use of individual polyps that bail-out of the coral skeleton induced by acute stress has been suggested as a model to study these processes. However, little is known about how these polyps change after bailing-out of a colony, which could become a problem once reliable models should be consistent and well understood. Thus, investigating these changes and optimizing a methodology to minimize them is crucial to establish these polyps as models to study corals. Herein, we investigated microbiological changes of isolated polyps by performing an experiment to study shifts in their microbiome after the separation from the colony. Before the experiment, different methods to isolate polyps were tested to find the one that granted the highest survival. After finding that salinity-induced separation was the most efficient, this method was used to study the microbiome of coral polyps. We found that while no significant changes in the microbiome could be observed immediately after the separation of polyps from their colony compared to coral fragments, this pattern changed after two weeks. We propose that the maintenance of polyps without fixation to a substrate might be the cause for such changes, and that polyps able to attach to a substrate and regrow as a colony might still recover a microbiome composition closer to coral fragments. Finally, a new microfluidic device for fixation and maintenance of coral polyps was developed and tested for use in future experiments.

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