Coral Calcification and Ocean Acidification

Abstract

Over 60 years ago, the discovery that light increased calcification in the coral plant-animal symbiosis triggered interest in explaining the phenomenon and understanding the mechanisms involved. Major findings along the way include the observation that carbon fixed by photosynthesis in the zooxanthellae is translocated to animal cells throughout the colony and that corals can therefore live as autotrophs in many situations. Recent research has focused on explaining the observed reduction in calcification rate with increasing ocean acidification (OA). Experiments have shown a direct correlation between declining ocean pH, declining aragonite saturation state (Ω_arag), declining [CO₃ ²⁻] and coral calcification. Nearly all previous reports on OA identify Ω_arag or its surrogate [CO₃ ²⁻] as the factor driving coral calcification. However, the alternate “Proton Flux Hypothesis” stated that coral calcification is controlled by diffusion limitation of net H⁺ transport through the boundary layer in relation to availability of dissolved inorganic carbon (DIC). The “Two Compartment Proton Flux Model” expanded this explanation and synthesized diverse observations into a universal model that explains many paradoxes of coral metabolism, morphology and plasticity of growth form in addition to observed coral skeletal growth response to OA. It is now clear that irradiance is the main driver of net photosynthesis (P_net), which in turn drives net calcification (G_net), and alters pH in the bulk water surrounding the coral. P_net controls [CO₃ ²⁻] and thus Ω_arag of the bulk water over the diel cycle. Changes in Ω_arag and pH lag behind G_net throughout the daily cycle by two or more hours. The flux rate P_net, rather than concentration-based parameters (e.g., Ω_arag, [CO₃ ²⁻], pH and [DIC]:[H⁺] ratio) is the primary driver of G_net. Daytime coral metabolism rapidly removes DIC from the bulk seawater. Photosynthesis increases the bulk seawater pH while providing the energy that drives calcification and increases in G_net. These relationships result in a correlation between G_net and Ω_arag, with both parameters being variables dependent on P_net. Consequently the correlation between G_net and Ω_arag varies widely between different locations and times depending on the relative metabolic contributions of various calcifying and photosynthesizing organisms and local rates of carbonate dissolution. High rates of H⁺ efflux continue for several hours following the mid-day G_net peak suggesting that corals have difficulty in shedding waste protons as described by the Proton Flux Model. DIC flux (uptake) tracks P_net and G_net and drops off rapidly after the photosynthesis-calcification maxima, indicating that corals can cope more effectively with the problem of limited DIC supply compared to the problem of eliminating H⁺. Predictive models of future global changes in coral and coral reef growth based on oceanic Ω_arag must include the influence of future changes in localized P_net on G_net as well as changes in rates of reef carbonate dissolution. The correlation between Ω_arag and G_net over the diel cycle is simply the result of increasing pH due to photosynthesis that shifts the CO₂-carbonate system equilibria to increase [CO₃ ²⁻] relative to the other DIC components of [HCO₃ ⁻] and [CO₂]. Therefore Ω_arag closely tracks pH as an effect of P_net, which also drives changes in G_net. Measurements of DIC flux and H⁺ flux are far more useful than concentrations in describing coral metabolism dynamics. Coral reefs are systems that exist in constant disequilibrium with the water column.

Appendix

Appendix Table 2.1 Data reported for A_T, Ca²⁺, CO₃ ²⁻, HCO₃ ⁻, Ω_arag, pH and G during each of the experimental trials (Langdon et al. 2000) and calculations for [DIC], [H⁺] and the [DIC]:[H⁺] ratio