Calcium carbonate (CaCO ₃ ) biomineralizing organisms have played major roles in the history of life and the global carbon cycle during the past 541 Ma. Both marine diversification and mass extinctions reflect physiological responses to environmental changes through time. An integrated understanding of carbonate biomineralization is necessary to illuminate this evolutionary record and to understand how modern organisms will respond to 21st century global change. Biomineralization evolved independently but convergently across phyla, suggesting a unity of mechanism that transcends biological differences. In this review, we combine CaCO ₃ skeleton formation mechanisms with constraints from evolutionary history, omics, and a meta-analysis of isotopic data to develop a plausible model for CaCO ₃ biomineralization applicable to all phyla. The model provides a framework for understanding the environmental sensitivity of marine calcifiers, past mass extinctions, and resilience in 21st century acidifying oceans. Thus, it frames questions about the past, present, and future of CaCO ₃ biomineralizing organisms.

Ocean acidification causes corals to calcify at reduced rates, but current understanding of the underlying processes is limited. Here, we conduct a mechanistic study into how seawater acidification alters skeletal growth of the coralStylophora pistillata. Reductions in colony calcification rates are manifested as increases in skeletal porosity at lower pH, while linear extension of skeletons remains unchanged. Inspection of the microstructure of skeletons and measurements of pH at the site of calcification indicate that dissolution is not responsible for changes in skeletal porosity. Instead, changes occur by enlargement of corallite-calyxes and thinning of associated skeletal elements, constituting a modification in skeleton architecture. We also detect increases in the organic matrix protein content of skeletons formed under lower pH. Overall, our study reveals that seawater acidification not only causes decreases in calcification, but can also cause morphological change of the coral skeleton to a more porous and potentially fragile phenotype.

The mechanisms behind the transfer of molecules from the surrounding sea water to the site of coral calcification are not well understood, but are critical for understanding how coral reefs are formed. We conducted experiments with the fluorescent dye calcein, which binds to calcium and is incorporated into growing calcium carbonate crystals, to determine the permeability properties of coral cells and tissues to this molecule, and to determine how it is incorporated into the coral skeleton. We also compared rates of calcein incorporation with rates of calcification measured by the alkalinity anomaly technique. Finally, by an electrophysiological approach, we investigated the electrical resistance of coral tissues in order to better understand the role of tissues in ionic permeability. Our results show that (i) calcein passes through coral tissues by a paracellular pathway, (ii) intercellular junctions control and restrict the diffusion of molecules, (iii) intercellular junctions should have pores of a size higher than 13 Å and lower than 20 nm, and (iv) the resistance of the tissues owing to paracellular junctions has a value of 477 ± 21 Ohm cm². We discuss the implication of our results for the transport of calcium involved in the calcification process.

In vivo measurements of [Ca ²⁺ ] and [CO ₃ ²⁻ ] indicate biological control of carbonate chemistry at site of calcification in corals.

This work, performed on the scleractinian coral Stylophora pistillata, aims at providing new information on the `light-enhanced calcification' process. In a first step, in controlled conditions of culture and constant light supply, we studied the diurnal cycle of calcification. We determined that calcification rates are constant during the day and the night with a 2.6-fold difference between day and night calcification rates. We also showed that the photosynthetic rate is constant throughout the day when a constant light intensity is applied. Our results on free-running experiments in prolonged conditions of light or dark suggest that calcification is not regulated by an endogenous circadian rhythm. In a second step, using a kinetic isotopic approach with ⁴⁵Ca, we characterized the transition stages between day and night and vice versa. Under our experimental conditions, the lag-phase necessary to switch from the light to the dark calcification rate is the same as the lag-phase necessary to switch from the dark to the light calcification rate. We discuss our results in the context of two hypotheses of the light-enhanced calcification process: (1) the role of photosynthesis on the pH in the coelenteron and (2) the role of photosynthesis in supplying precursors of the organic matrix.