The declining health of coral reefs worldwide is likely to intensify in response to continued anthropogenic disturbance from coastal development, pollution, and climate change. In response to these stresses, reef-building corals may exhibit bleaching, which marks the breakdown in symbiosis between coral and zooxanthellae. Mass coral bleaching due to elevated water temperature can devastate coral reefs on a large geographical scale. In order to understand the molecular and cellular basis of bleaching in corals, we have measured gene expression changes associated with thermal stress and bleaching using a complementary DNA microarray containing 1310 genes of the Caribbean coral Montastraea faveolata. In a first experiment, we identified differentially expressed genes by comparing experimentally bleached M. faveolata fragments to control non-heat-stressed fragments. In a second experiment, we identified differentially expressed genes during a time course experiment with four time points across 9 days. Results suggest that thermal stress and bleaching in M. faveolata affect the following processes: oxidative stress, Ca 2+ homeostasis, cytoskeletal organization, cell death, calcification, metabolism, protein synthesis, heat shock protein activity, and transposon activity. These results represent the first medium-scale transcriptomic study focused on revealing the cellular foundation of thermal stress-induced coral bleaching. We postulate that oxidative stress in thermal-stressed corals causes a disruption of Ca 2+ homeostasis, which in turn leads to cytoskeletal and cell adhesion changes, decreased calcification, and the initiation of cell death via apoptosis and necrosis.

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Coral reefs are degrading worldwide at an alarming rate. Nutrient over-enrichment is considered a major cause of this decline because degraded coral reefs generally exhibit a shift from high coral cover (low algal cover) to low coral cover with an accompanying high cover and biomass of fleshy algae. Support for such claims is equivocal at best. Critical examination of both experimental laboratory and field studies of nutrient effects on corals and coral reefs, including the Elevated Nutrient on Coral Reefs Experiment (ENCORE) enrichment experiment conducted on the Great Barrier Reef, does not support the idea that the levels of nutrient enrichment documented at anthropogenically-enriched sites can affect the physiology of corals in a harmful way, or for most cases, be the sole or major cause of shifts in coralalgal abundance. Factors other than nutrient enrichment can be significant causes of coral death and affect algal cover, and include decreased abundance of grazing fishes by fishing, and of grazing sea urchins to disease; grazing preferences of remaining grazers; temperature stress that kills coral (i.e., coral bleaching) and creates more open substrate for algal colonization; sedimentation stress that can weaken adult corals and prevent coral recruitment; coral diseases that may be secondary to coral bleaching; and outbreaks of coral predators and sea urchins that may be secondary effects of overfishing. Any factor that leads to coral death or reduces levels of herbivory will leave more substrate open for algal colonization or make the effects of even low-level enrichment more severe. Factors that contribute to an imbalance between production and consumption will result in community structure changes similar to those expected from overenrichment. Over-enrichment can be and has been the cause of localized coral reef degradation, but the case for widespread effects is not substantiated.

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Coral reefs are based on the symbiotic relationship between corals and photosynthetic dinoflagellates of the genus Symbiodinium. We followed gene expression of coral larvae of Acropora palmata and Montastraea faveolata after exposure to Symbiodinium strains that differed in their ability to establish symbioses. We show that the coral host transcriptome remains almost unchanged during infection by competent symbionts, but is massively altered by symbionts that fail to establish symbioses. Our data suggest that successful coral-algal symbioses depend mainly on the symbionts' ability to enter the host in a stealth manner rather than a more active response from the coral host.

BackgroundCoral reefs are expected to be severely impacted by rising seawater temperatures associated with climate change. This study used cDNA microarrays to investigate transcriptional effects of thermal stress in embryos of the coral Montastraea faveolata. Embryos were exposed to 27.5°C, 29.0°C, and 31.5°C directly after fertilization. Differences in gene expression were measured after 12 and 48 hours.ResultsAnalysis of differentially expressed genes indicated that increased temperatures may lead to oxidative stress, apoptosis, and a structural reconfiguration of the cytoskeletal network. Metabolic processes were downregulated, and the action of histones and zinc finger-containing proteins may have played a role in the long-term regulation upon heat stress.ConclusionsEmbryos responded differently depending on exposure time and temperature level. Embryos showed expression of stress-related genes already at a temperature of 29.0°C, but seemed to be able to counteract the initial response over time. By contrast, embryos at 31.5°C displayed continuous expression of stress genes. The genes that played a role in the response to elevated temperatures consisted of both highly conserved and coral-specific genes. These genes might serve as a basis for research into coral-specific adaptations to stress responses and global climate change.

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