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Abstract Historically mechanisms with which basal animals such as reef-building corals use to respond to changing and increasingly stressful environments have remained elusive. However, the increasing availability of genomic and transcriptomic data from these organisms has provided fundamental insights into the biology of these critically important ecosystem engineers. Notably, insights into cnidarians gained in the post-genomics age have revealed a surprisingly complex immune system which bears a surprising level of similarity with the vertebrate innate immune system. This system has been critically linked to how corals respond to the two most prominent threats on a global scale, emerging coral diseases and increasing water temperature, which are recognized cellularly as either foreign or domestic threats, respectively. These threats can arise from pathogenic microbes or internal cellular dysfunction, underscoring the need to further understand mechanisms corals use to sense and respond to threats to their cellular integrity. In this investigation and meta-analysis, we utilize resources only recently available in the post-genomic era to identify and characterize members of an underexplored class of molecules known as NOD-like receptors in the endangered Caribbean coral Orbicella faveolata. We then leverage these data to identify pathways possibly mediated by NLRs in both O. faveolata and the ecologically important branching coral Acropora digitifera. Overall, we find support that this class of proteins may provide a mechanistic link to how reef-building corals respond to threats both foreign and domestic. 

Abstract As scleractinian coral cover declines in the face of increased frequency in disease outbreaks, future reefs may become dominated by octocorals. Understanding octocoral disease responses and consequences is therefore necessary if we are to gain insight into the future of ecosystem services provided by coral reefs. In Florida, populations of the octocoral Eunicea calyculata infected with Eunicea black disease (EBD) were observed in the field in the fall of 2011. This disease was recognized by a stark, black pigmentation caused by heavy melanization. Histological preparations of E. calyculata infected with EBD demonstrated granular amoebocyte (GA) mobilization, melanin granules in much of the GA population, and the presence of fungal hyphae penetrating coral tissue. Previous transcriptomic analysis also identified immune trade-offs evidenced by increased immune investment at the expense of growth. Our investigation utilized proteogenomic techniques to reveal decreased investment in general cell signaling while increasing energy production for immune responses. Inflammation was also prominent in diseased E. calyculata and sheds light on factors driving the extreme phenotype observed with EBD. With disease outbreaks continuing to increase in frequency, our results highlight new targets within the cnidarian immune system and provide a framework for understanding transcriptomics in the context of an organismal disease phenotype and its protein expression.