TitleDevelopment of symbiosis-specific genes as biomarkers for the early detection of cnidarian-algal symbiosis breakdown
Publication TypeJournal Article
Year of Publication2002
AuthorsMitchelmore, CL, Schwarz, JA, Weis, VM
JournalMarine Environmental Research
Volume54
Pagination345-349
Type of ArticleJournal Article
ISSN0141-1136
Abstract

Coral bleaching, i.e. the loss of dinoflagellate symbionts from cnidarian hosts, is occurring globally at increasing rates, scales, and severity. The significance of these bleaching events to the health of coral reef ecosystems is extreme, as bleached corals exhibit high mortality, reduced fecundity, and productivity and increased susceptibility to disease. This decreased coral fitness leads to reef degradation and ultimately to the breakdown of the coral reef ecosystem. To date,there has been little work describing the application of biomarkers to assess coral health. The most commonly applied biomarker is, in fact, the bleaching event itself. We are interested in developing early warning biomarkers that can detect coral stress before bleaching occurs. Recently, several genes that are likely to function in regulating interactions between cnidarians and their symbionts have been characterized, using the temperate sea anemone Anthopleura elegantissima as a model species. One "symbiosis gene" identified from the host genome, sym32, is expressed as a function of anemone symbiotic-state, where sym32 expression is higher in symbiotic cf. aposymbiotic (symbiont-free) anemones. Real-time quantitative RT-PCR suggested that the level of sym32 expression was correlated with the abundance of algae in the host. Furthermore, laboratory exposures of anemones to low levels of cadmium (0, 20, 100 mug(-1) CdCl2; 14 days), which caused no change in algal cell numbers, resulted in a down-regulation of sym32 compared to controls, indicating that sym32 expression may serve as a new sensitive early warning biomarker of cnidarian-algal symbiosis breakdown. (C) 2002 Elsevier Science Ltd. All rights reserved.

URL<Go to ISI>://WOS:000178360100026
DOI10.1016/s0141-1136(02)00201-5