MEPS 460:277-287 (2012)  -  DOI: https://doi.org/10.3354/meps09776

ABSTRACT: Toxins that open cell membrane calcium channels have been found in the dinoflagellate genus Symbiodinium, and likely occur in most zooxanthellae. I used published observations to examine some potentially far-reaching consequences to reef corals. Algal toxins may stimulate coral calcification by opening Ca²⁺ channels on the calcifying ectoderm. The coral discharges the resulting protons (Ca²⁺ + HCO₃⁻ → CaCO₃ + H⁺) into its coelenteron cavity, where they improve algal bicarbonate and nutrient assimilation. Coupling calcification with autotrophic physiologies contributes to the success of highly calcareous zooxanthellar symbioses, and to their associations with nutrient-poor tropical waters. Nutrient shortages freeze zooxanthellae in the G1 phase of the cell cycle. Dinoflagellates are often most toxic at such times, perhaps because toxins modulate their nuclear mix of cations, to control DNA conformation and activity. Increased Ca²⁺ influx into host cells disrupts cell adhesion and induces apoptosis. Zooxanthellae assimilate host nutrients, complete G1, divide, and disperse to new hosts. Nutrient shortages associate with high sea surface temperatures (SST), producing correlations between SST, calcification, and algal exit. Zooxanthellae proliferate when nutrients are abundant, but when nutrients later disappear, usually as SST warms, toxins and the departure of over-abundant zooxanthellae potentially overwhelm the coral and cause coral bleaching.

KEY WORDS: Toxin · Coral · Polyketide · Symbiodinium · Calcification · Photosynthesis · Bleaching