Stony coral tissue loss disease (SCTLD) was initially documented in Florida in 2014 and outbreaks with similar characteristics have since appeared in disparate areas throughout the northern Caribbean, causing significant declines in coral communities. SCTLD is characterized by focal or multifocal lesions of denuded skeleton caused by rapid tissue loss and affects at least 22 reef-building species of Caribbean corals. A tissue-loss disease consistent with the case definition of SCTLD was first observed in the U.S. Virgin Islands (USVI) in January of 2019 off the south shore of St. Thomas at Flat Cay. The objective of the present study was to characterize species susceptibility to the disease present in St. Thomas in a controlled laboratory transmission experiment. Fragments of six species of corals (Colpophyllia natans, Montastraea cavernosa, Orbicella annularis, Porites astreoides, Pseudodiploria strigosa, and Siderastrea siderea) were simultaneously incubated with (but did not physically contact) SCTLD-affected colonies of Diploria labyrinthiformis and monitored for lesion appearance over an 8 day experimental period. Paired fragments from each corresponding coral genotype were equivalently exposed to apparently healthy colonies of D. labyrinthiformis to serve as controls; none of these fragments developed lesions throughout the experiment. When tissue-loss lesions appeared and progressed in a disease treatment, the affected coral fragment, and its corresponding control genet, were removed and preserved for future analysis. Based on measures including disease prevalence and incidence, relative risk of lesion development, and lesion progression rates, O. annularis, C. natans, and S. siderea showed the greatest susceptibility to SCTLD in the USVI. These species exhibited earlier average development of lesions, higher relative risk of lesion development, greater lesion prevalence, and faster lesion progression rates compared with the other species, some of which are considered to be more susceptible based on field observations (e.g., P. strigosa). The average transmission rate in the present study was comparable to tank studies in Florida, even though disease donor species differed. Our findings suggest that the tissue loss disease affecting reefs of the USVI has a similar epizootiology to that observed in other regions, particularly Florida.

Disease outbreaks have caused significant declines of keystone coral species. While forecasting disease outbreaks based on environmental factors has progressed, we still lack a comparative understanding of susceptibility among coral species that would help predict disease impacts on coral communities. The present study compared the phenotypic and microbial responses of seven Caribbean coral species with diverse life-history strategies after exposure to white plague disease. Disease incidence and lesion progression rates were evaluated over a seven-day exposure. Coral microbiomes were sampled after lesion appearance or at the end of the experiment if no disease signs appeared. A spectrum of disease susceptibility was observed among the coral species that corresponded to microbial dysbiosis. This dysbiosis promotes greater disease susceptiblity in coral perhaps through different tolerant thresholds for change in the microbiome. The different disease susceptibility can affect coral’s ecological function and ultimately shape reef ecosystems.

Pattern recognition receptors (PRRs) are evolutionarily ancient and crucial components of innate immunity, recognizing danger-associated molecular patterns (DAMPs) and activating host defenses. Basal non-bilaterian animals such as cnidarians must rely solely on innate immunity to defend themselves from pathogens. By investigating cnidarian PRR repertoires we can gain insight into the evolution of innate immunity in these basal animals. Here we utilize the increasing amount of available genomic resources within Cnidaria to survey the PRR repertoires and downstream immune pathway completeness within 15 cnidarian species spanning two major cnidarian clades, Anthozoa and Medusozoa. Overall, we find that anthozoans possess prototypical PRRs, while medusozoans appear to lack these immune proteins. Additionally, anthozoans consistently had higher numbers of PRRs across all four classes relative to medusozoans, a trend largely driven by expansions in NOD-like receptors and C-type lectins. Symbiotic, sessile, and colonial cnidarians also have expanded PRR repertoires relative to their non-symbiotic, mobile, and solitary counterparts. Interestingly, cnidarians seem to lack key components of mammalian innate immune pathways, though similar to PRR numbers, anthozoans possess more complete immune pathways than medusozoans. Together, our data indicate that anthozoans have greater immune specificity than medusozoans, which we hypothesize to be due to life history traits common within Anthozoa. Overall, this investigation reveals important insights into the evolution of innate immune proteins within these basal animals.

Stony coral tissue loss disease (SCTLD), one of the most pervasive and virulent coral diseases on record, affects over 22 species of reef-building coral and is decimating reefs throughout the Caribbean. To understand how different coral species and their algal symbionts (family Symbiodiniaceae) respond to this disease, we examine the gene expression profiles of colonies of five species of coral from a SCTLD transmission experiment. The included species vary in their purported susceptibilities to SCTLD, and we use this to inform gene expression analyses of both the coral animal and their Symbiodiniaceae. We identify orthologous coral genes exhibiting lineage-specific differences in expression that correlate to disease susceptibility, as well as genes that are differentially expressed in all coral species in response to SCTLD infection. We find that SCTLD infection induces increased expression of rab7, an established marker of in situ degradation of dysfunctional Symbiodiniaceae, in all coral species accompanied by genus-level shifts in Symbiodiniaceae photosystem and metabolism gene expression. Overall, our results indicate that SCTLD infection induces symbiophagy across coral species and that the severity of disease is influenced by Symbiodiniaceae identity.

The Anthropocene will be characterized by increased environmental disturbances, leading to the survival of stress-tolerant organisms, particularly in the oceans, where novel marine diseases and elevated temperatures are re-shaping ecosystems. These environmental changes underscore the importance of identifying mechanisms which promote stress tolerance in ecologically important non-model species such as reef-building corals. Mitochondria are central regulators of cellular stress and have dedicated recovery pathways including the mitochondrial unfolded protein response, which increases the transcription of protective genes promoting protein homeostasis, free radical detoxification and innate immunity. In this investigation, we identify a mitochondrial unfolded protein response in the endangered Caribbean coral Orbicella faveolata , by performing in vivo functional replacement using a transcription factor (Of-ATF5) originating from a coral in the model organism Caenorhabditis elegans . In addition, we use RNA-seq network analysis and transcription factor-binding predictions to identify a transcriptional network of genes likely to be regulated by Of-ATF5 which is induced during the immune challenge and temperature stress. Overall, our findings uncover a conserved cellular pathway which may promote the ability of reef-building corals to survive increasing levels of environmental stress.