'White syndrome' is considered to be the most prevalent coral disease on the Great Barrier Reef, characterised by rapid rates of lesion progression and high levels of colony mortality. This study investigated the production and translocation of photoassimilates towards white syndrome lesions (WSLs) and artificially inflicted lesions in healthy and diseased colonies of tabular Acropora spp. to determine the intra-colonial response to white syndrome using 14C labelling. Translocation of 14C labelled photoassimilates was preferentially orientated away from active WSLs, with minimal 14C activity observed in the lesion borders, whilst artificial lesions (ALs) created directly opposite WSL borders showed significantly higher 14C activity, suggesting active translocation of photoassimilates for tissue regeneration. Transport of photoassimilates in healthy coral colonies was preferentially oriented towards ALs with a higher perimeter-area ratio, although translocation towards WSL boundaries was minimal even though the lesion perimeter was often the width of the colony (> 200 cm). We suggest that the preferential orientation of photoassimilates away from WSLs may represent a deliberate strategy by the colony to induce a 'shutdown reaction' in order to preserve intra-colonial resources within areas of the colony that are more likely to survive and recover.
Bibliographical noteFunding Information:
Acknowlegements The authors are grateful to the World Bank GEF Coral Reef Targeted Research Program (http://www.gefcoral.org) and the ARC Discovery program for support during this study. They are also grateful for the support provided by the staff of Heron Island Research Station as well as the members of the Marine Animal Plant Symbiosis Laboratory.
- Resource translocation
- White syndrome