33-3 Sat Jan 2 Physiological and transcriptomic responses of Caribbean corals under global change Bove, CB*; Davies, SW; Ries, JB; Umbanhowar, J; Castillo, KD; UNC Chapel Hill and Boston University; Boston University; Northeastern University; UNC Chapel Hill; UNC Chapel Hill colleenbove@gmail.com
Continued ocean acidification and warming is a major concern for marine organisms, especially for reef-building corals that rely on their symbiotic relationship with algae, which is highly susceptible to perturbation. Coral physiological responses to global change stressors, at the individual and species levels, will ultimately determine the future of tropical reefs. Here, we investigated the combined effects of chronic acidification (280−3300 µatm) and warming (28, 31 °C) (95 days) on the physiological responses of three species of coral hosts and their algal symbionts (Siderastrea siderea, Pseudodiploria strigosa, Porites astreoides) from the Belize Mesoamerican Barrier Reef System. To explore the molecular underpinnings of these responses, gene expression of S. siderea was profiled. Warming more negatively impacted S. siderea host physiology, while symbiont physiology declined under acidification. Preliminary gene expression analyses suggest transcriptome resilience to stressors. Warming negatively impacted the majority of P. strigosa host and symbiont traits, while host traits and chlorophyll a concentrations in P. astreoides were negatively affected by increasing acidification. Principal component analyses revealed that differences in overall coral physiology of all three species were affected by ocean acidification, while warming only impacted P. strigosa. These results demonstrate that while ocean warming is a severe acute stressor that will have dire consequences for coral reefs globally, chronic exposure to acidification may be impacting coral physiology to a greater extent than previously assumed. Understanding variation in responses is critical to predicting the future of Caribbean reefs as global change unfolds.