Abstract
Coral disease is a global phenomenon, with the Caribbean noted as a coral disease hotspot. White band disease is the key driver of decline of the keystone Caribbean coral species Acropora palmata. Despite the large-scale reduction in coral cover, our understanding of the transcriptomic and bacterial microbiome disease responses in A. palmata is not well understood. This includes not knowing the causative pathogen(s) of white band disease, the transcriptomic response of the coral host to differing disease inoculations, the dynamics of the microbiome, and how heat stress influences disease susceptibility. This Ph.D. identified the disease dynamics of A. palmata inoculated with different diseases and how this affected the coral hosts transcriptomic and bacterial response. Characterisation of the coral hosts transcriptomic response was also identified for outplanted A. palmata to identify whether identified disease responses could be captured in an ex-situ environment. I found that A. palmata exhibits a strong transcriptomic response to disease inoculation that is highly similar to other coral species, namely the activation of a strong innate immune response. Despite differing disease types, and time of inoculations, a common response was identified at a transcriptomic level, with this dominated by genes important in innate immunity. Short term heat stress did not affect disease incidence, indicating longer term heat stress events may be required to increase disease susceptibility. The bacterial microbiome also showed a common response to different disease inoculations, indicating that manifestation of visual disease signs may be due to a successional shift from healthy to a diseased state. There were clear transcriptomic profiles of outplanted A. palmata over a year period, with gene sets showing high similarity during the warmer summer months with gene sets identified in disease inoculated corals. This dissertation has provided an in-depth characterization of the coral hosts transcriptomic and bacterial component of the microbiome response to disease in A. palmata.