| Summary: | Coral communities around the world are projected to be negatively affected by ocean acidification. Not all coral species will respond in the same manner to rising CO2 levels. Evidence from naturally acidified areas such as CO2 seeps have shown that although a few species are resistant to elevated CO2, most lack sufficient resistance resulting in their decline. This has led to the simple grouping of coral species into "winners" and "losers," but the physiological traits supporting this ecological assessment are yet to be fully understood. Here using CO2 seeps, in two biogeographically distinct regions, we investigated whether physiological traits related to energy production [mitochondrial electron transport systems (ETSAs) activities] and biomass (protein contents) differed between winning and losing species in order to identify possible physiological traits of resistance to ocean acidification and whether they can be acquired during shortterm transplantations. We show that winning species had a lower biomass (protein contents per coral surface area) resulting in a higher potential for energy production (biomass specific ETSA: ETSA per protein contents) compared to losing species. We hypothesize that winning species inherently allocate more energy toward inorganic growth (calcification) compared to somatic (tissue) growth. In contrast, we found that losing species that show a higher biomass under reference pCO(2) experienced a loss in biomass and variable response in area-specific ETSA that did not translate in an increase in biomass-specific ETSA following either short-term (4-5 months) or even lifelong acclimation to elevated pCO(2) conditions. Our results suggest that resistance to ocean acidification in corals may not be acquired within a single generation or through the selection of physiologically resistant individuals. This reinforces current evidence suggesting that ocean acidification will reshape coral communities around the world, selecting species that have an inherent resistance to elevated pCO(2).
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