Respiratory electron transport system activity in symbiotic corals and its link to calcification

Abstract

Scleractinian corals host photosynthetic endosymbionts, making direct measurement of the host respiration rate via incubation methods based on O2 consumption impossible. We tested the use of the respiratory electron transport system activity (ETSA) for measuring host potential respiration. The applied method, modified from a previous study, is based on the re - duction of (4-iodophenyl)-3-(4-nitrophenyl)-5-phenyl-2H-tetrazolium chloride (INT) to formazan. After the development of a protocol suitable for corals, the method was tested on 5 different spe- cies. Metabolism, including photosynthesis, dark respiration and light and dark calcification, was measured through incubation. Host and zooxanthellae fractions were separated and their ETSAs, protein contents and zooxanthellae densities were measured. Mean ETSA/dark respiration (ETSA/R) ratios for host corals ranged from 1.7 ± 0.2 to 3.5 ± 0.6, while ratios for zooxanthellae ranged from 3.7 to 7.8. The high ratios observed for zooxanthellae indicate that their respiration may be 5 times higher under light conditions than in the dark. Considering the obtained ratios, host respiration in light could increase at most by a factor of 3.5 compared with dark respiration rates. Ratios close to 1 were found for some specimens, which suggests that higher respiration rates under light compared with dark conditions are not possible. Therefore, increased respiration in light cannot explain the observed enhancement of calcification under light conditions. ETSA was correlated with zooxanthellae density, suggesting adaptation of the levels of host ETS enzymes to the amount of translocated photosynthetates under optimal conditions. Estimated dark host respiration was correlated with photosynthesis, which suggests that it is determined mainly by the amount of energy available but also the amount of electron transport system enzymes. This constrains the amount of ATP available for calcification. Hence, we propose a mechanism by which respiration limits the calcification rate.