Up to 98 % of the total carbon acquired by scleractinian anthozoans (coral) is provided by carbon fixation from an algal symbiont (Symbiodinium spp.). In return, the host provides protection, a source of nitrogen, and CO2 for carbon fixation to the symbiont. The obligate nature of this symbiosis places constraints on the environmental conditions capable of sustaining growth, reproduction, and reef expansion. Although many environmental factors can be detrimental to corals climate warming and disease have drastically altered coral communities over the past 40 years. Coral cover along the Florida Reef Tract (FRT) has decreased by 70 % and as a result the benthic reef community has transitioned from a coral dominated to a macro-algal dominated ecosystem. The primary contributors to the observed phase shift are disease and climate change. Increasing our understanding of coral resistance and sensitivity to disease and climate change related stressors is paramount when the future of this ecosystem is considered. Differential habitation of the inshore patch reef system and offshore bank reef system is identified with a multivariate statistical approach among three coral species, Porites astreoides, Montastraea cavernosa, and Siderastrea siderea. All three species were observed to have increased size and abundance at inshore reefs despite the characterization of inshore patch reefs as a habitat with increased levels of thermal stress and eutrophication compared to offshore bank reef habitats. These results point to disease as a contributing factor affecting the offshore bank reef system. Based on the extensive history of disease associated with the offshore bank reef system, I hypothesized that offshore coral communities increase immune expression to deter disease. Because corals utilize an innate immune system to detect and respond to harmful microorganisms, I applied quantitative reverse transcription real-time PCR of genes associated with immunity to estimate the degree of this response. Reciprocal transplantation of P. astreoides collected from a representative inshore and offshore reef enabled the distinction between environmental and population dependent effects. Upregulation of TNF receptor associated factor 3, a protein critical to bacterial and viral responses, was identified in corals experiencing the offshore habitat during the summer indicating increased disease related stress during warmer periods. Corals originating offshore upregulated expression of adenylate cyclase associated protein 2 compared to inshore corals indicating an adaptive response to increased disease related stress. Population-dependent adaptive responses to temperature and pathogen related stress in P. astreoides were confirmed by challenging fragments originating from each site (n = 6) for 8 h with a control (28°C), increased temperature (32°C), or a treatment of increased seawater temperature and 5 μg ml-1 lipopolysaccharide. Offshore coral fragments exposed to the synergistic treatment and inshore coral fragments exposed to increased SWT displayed responsive upregulation of genes. Responsive upregulation of genes was associated with increased variation in SWT for inshore corals and increased variation in pathogen associated molecular patterns response in offshore corals. The observed increase in expression of the immune system by the offshore population was also associated with decreased coral abundance (survival) and decreased colony size, which in P. astreoides contributes to decreased fecundity. Therefore, survival of offshore corals in the face of pathogenic organisms likely comes at costs to other measures of fitness whereas inshore corals do not experience these pathogen related costs. Therefore, two populations of P. astreoides inhabit the FRT. As SWTs continue to increase from carbon emissions, thermal stress will likely exacerbate the effects of pathogen related stress impacting the offshore population and SWT stress will further impact the inshore population. Both populations are in peril but we identify pathogen associated stress as a concealed stressor.
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