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Mol Ecol. 2009 Dec;18(24):5101-14. doi: 10.1111/j.1365-294X.2009.04419.x. Epub 2009 Nov 9.

Early molecular responses of coral larvae to hyperthermal stress.

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Department of Biology, University of Louisiana at Lafayette, 70504, USA.

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  • Mol Ecol. 2010 Mar;19(5):1071.


Most of the work on the impact of elevated temperature and light on Symbiodinium-invertebrate symbioses have focused primarily on how the photosynthetic (algal) partner is impacted. Understanding how the same stresses affect the invertebrate host, however, is in its infancy. In this study, we re-examined the direct effect of elevated temperatures on the invertebrate host exploring the early transcriptional response of aposymbiotic (without algal symbionts) coral larvae. The temperatures tested in the experimental design were 24 degrees C (ambient seawater temperature), 28 degrees C and 31 degrees C; and the sampling points were 3 and 10 h after temperature exposure. We explored relative changes in transcription using a cDNA microarray constructed for the scleractinian coral, Acropora millepora, and containing 18 142 expressed sequence tag (EST) clones/8386 unigenes. Our study identified 29 genes that were significantly up- and down-regulated when A. millepora coral larvae were exposed to elevated temperatures. Down-regulation of several key components of DNA/RNA metabolism was detected implying inhibition of general cellular processes. The down-regulation of protein synthesis, however, was not simple and random, which suggested that the stress response was a more complicated adjustment of cellular metabolism. We identified four significant outcomes during the very early hours of the transcriptional response to hyperthermal stress in coral larvae. First, the expression of heat-shock proteins increased rapidly (within 3 h) in response to hyperthermal stress. Second, a fluorescent protein homologue, DsRed-type FP, decreased its expression in response to elevated temperature reinforcing a potential role as a molecular marker for monitoring hyperthermal stress in nature. Third, the down-regulation of a coral mannose-binding C-type lectin under elevated temperature suggests that heat stress might compromise some components of the coral immune defence and therefore might bring about susceptibility to pathogenic diseases. And last, genes involved in protecting cells against oxidative stress showed little response at the early hours to heat stress, supporting the proposal that up-regulation of cnidarian host oxidative stress genes may require reactive oxygen species generated by stressed algal symbionts.

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