DAO 117:155-163 (2015)  -  DOI: https://doi.org/10.3354/dao02882

ABSTRACT: White syndrome has been described as one of the most prolific diseases on the Great Barrier Reef. Previously, apoptotic cell death has been described as the mechanism driving the characteristic rapid tissue loss associated with this disease, but the molecular mechanisms controlling apoptotic cell death in coral disease have yet to be investigated. In situ methods were used to study the expression patterns of 2 distinct regulators of apoptosis in Acropora hyacinthus tissues undergoing white syndrome and apoptotic cell death. Apoptotic genes within the Bcl-2 family were not localized in apparently healthy coral tissues. However, a Bcl-2 family member (bax-like) was found to localize to cells and tissues affected by white syndrome and those with morphological evidence for apoptosis. A potential up-regulation of pro-apoptotic or bax-like gene expression in tissues with apoptotic cell death adjacent to disease lesions is consistent with apoptosis being the primary cause of rapid tissue loss in coral affected by white syndrome. Pro-apoptotic (bax-like) expression in desmocytes and the basal tissue layer, the calicodermis, distant from the disease lesion suggests that apoptosis may also underlie the sloughing of healthy tissues associated with the characteristic, rapid spread of tissue loss, evident of this disease. This study also shows that in situ hybridisation is an effective tool for studying gene expression in adult corals, and wider application of these methods should allow a better understanding of many aspects of coral biology and disease pathology.

KEY WORDS: Gene expression · In situ hybridisation · Coral disease · White syndrome · Apoptosis · Acropora

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Cite this article as: Ainsworth TD, Knack B, Ukani L, Seneca F, Weiss Y, Leggat W (2015) In situ hybridisation detects pro-apoptotic gene expression of a Bcl-2 family member in white syndrome-affected coral. Dis Aquat Org 117:155-163. https://doi.org/10.3354/dao02882 Export citation Share:    Facebook - - linkedIn