That corals skeletons are built of aragonite crystals with taxonomy-linked ultrastructure has been well understood since the 19th century. Yet, the way by which corals control this crystallization process remains an unsolved question. Here, I outline a new conceptual model of coral biominerationsation that endeavours to relate known skeletal features with homeostatic functions beyond traditional growth (structural) determinants. In particular, I propose that the dominant physiological driver of skeletal extension is night-time hypoxia, which is exacerbated by the respiratory oxygen demands of the coral’s algal symbionts (= zooxanthellae). The model thus provides a new narrative to explain the high growth rate of symbiotic corals, by equating skeletal deposition with the “work-rate” of the coral host needed to maintain a stable and beneficial symbiosis. In this way, coral skeletons are interpreted as a continuous (long-run) recording unit of the stability and functioning of the coral-algae endosymbiosis. After providing supportive evidence for the model across multiple scales of observation, I use coral core data from the Great Barrier Reef (Australia) to highlight the disturbed nature of the symbiosis in recent decades, but suggest that its onset is consistent with a trajectory that has been followed since at least the start of the 1900′s. In concluding, I explain how the evolved capacity of the cnidarians (which now includes modern reef corals) to overcome the metabolic limitation of hypoxia via skeletogenesis, may underpin the sudden appearance in the fossil record of calcified skeletons at the Precambrian-Cambrian transition – and the ensuing rapid appearance of most major animal phyla.
Wooldridge S. A., 2012. A new conceptual model of coral biomineralisation: hypoxia as the physiological driver of skeletal extension. Biogeosciences Discussions 9: 12627-12666. Article.