Meeting Abstract
Marine diseases affecting reef building corals have radically transformed Caribbean reef ecosystems where disease-resistant species are favored to persist. In order to respond to pathogenic microbes, corals possess a well-stocked innate immune arsenal, and recent evidence indicates that like model organisms their innate immune system is regulated in large part by mitochondrial function. To investigate inter-species disease resistance mechanisms, we conducted a disease transmission experiment of the coral disease White Plague (WP) between two closely related species of coral: Orbicella faveolata, and Montastrea cavernosa. We found that O. faveolata is highly susceptible to this disease while M. cavernosa appears to be completely resistant in a laboratory setting. By using a comparative transcriptomics approach, we find a set of genes that are differentially expressed during disease exposure in both species. This analysis highlights a largely conserved response to disease including oxidative bursts and mitochondrial dysfunction. By applying a network-based gene expression analysis we also identify sets of genes with species-biased expression patterns which indicate differential regulation of mitochondrial genes. Additionally, pathway level analysis shows that these species activate and repress alternate pathways and regulatory molecules when challenge with White Plague. Overall, this investigation indicates that differential regulation of mitochondrial processes and subsequent employment of alternative cellular pathways during disease exposure may underlie the divergent disease resistance phenotypes between these two species.
