| Summary: | With escalating effects of global climate change, multiple abiotic stressors threaten the persistence of tropical coral reefs. Climate change has been shown to increase the biomass of macroalgae on coral reef ecosystems, thereby altering the benthic community structure. Ocean acidification, rising sea surface temperatures, and increasing irradiance affect the physiological processes and mechanisms of inorganic carbon uptake on macroalgae. However, the response of macroalgae to these abiotic stressors can be species-specific due to the physiological mechanisms by which macroalgae utilize CO2 or HCO3- from seawater, otherwise known as CO2 concentrating mechanisms (CCMs). This thesis examined the effects of variable abiotic stressors on the physiology of three tropical fleshy macroalgae (Sargassum pacificum, Turbinaria ornata, and Amansia rhodantha) in separate mesocosm studies for each algal species. Photosynthetic rates, growth, and CCM activity of S. pacificum and T. ornata were measured at ambient 400 µatm/27 °C and elevated 1000 µatm/30 °C conditions for each species. Physiological responses differed between the two species. Photosynthetic rates of T. ornata were constant across all pCO2 and temperature conditions, while growth rate decreased significantly with elevated temperature and CO2 supply. S. pacificum exhibited no significant difference in growth rates under elevated pCO2 and temperature, but a marginal increase in photosynthetic rates with increasing temperature and elevated pCO2. These results indicate that productivity of S. pacificum might exceed that of T. ornata under elevated pCO2 and temperature conditions. To explore the effects of light on the physiological mechanisms of macroalgae, a facultative CO2 user, Amansia rhodantha, was exposed to varying light regimes in a 12-day mesocosm study. Photosynthetic rates, growth, and inorganic carbon uptake were measured at ~600 µmol quanta m-2 s-1 and ~20 µmol quanta m-2 s-1. Photosynthetic rates decreased with each stepwise inclusion of CCM inhibitors ...
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