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SPATIAL HETEROGENEITY OF PHOTOSYNTHETIC ACTIVITY WITHIN DISEASED CORALS FROM THE GREAT BARRIER REEF1
Article first published online: 14 APR 2008
© 2008 Phycological Society of America
Journal of Phycology
Volume 44, Issue 2, pages 526–538, April 2008
How to Cite
Roff, G., Ulstrup, K. E., Fine, M., Ralph, P. J. and Hoegh-Guldberg, O. (2008), SPATIAL HETEROGENEITY OF PHOTOSYNTHETIC ACTIVITY WITHIN DISEASED CORALS FROM THE GREAT BARRIER REEF. Journal of Phycology, 44: 526–538. doi: 10.1111/j.1529-8817.2008.00480.x
Received 25 December 2006. Accepted 13 August 2007.
- Issue published online: 14 APR 2008
- Article first published online: 14 APR 2008
- chlorophyll a fluorescence;
- pulse-amplitude-modulated fluorometry;
- rapid light curves;
- symbiotic dinoflagellates;
- white syndrome;
Morphological diagnosis and descriptions of seven disease-like syndromes affecting scleractinian corals were characterized from the southern Great Barrier Reef (GBR). Chl a fluorescence of PSII was measured using an Imaging-PAM (pulse amplitude modulated) fluorometer, enabling visualization of the two-dimensional variability in the photophysiology of endosymbiotic dinoflagellates (zooxanthellae) by measuring rapid light curves. Three of four syndromes associated with active tissue loss (type a) were spatially homogenous (white syndrome, brown band, and skeletal eroding band), with no impact on the photochemical function of zooxanthellae populations at or behind the lesion borders. However, a decline in maximum quantum yield (Fv/Fm) and elevated levels of maximum nonphotochemical quenching (NPQmax) occurred in visually healthy tissue of black band disease adjacent to the lesion borders, possibly due to hypoxic conditions caused by the black band cyanobacterial mat. Two out of three syndromes associated with pathological change of intact tissue with no active tissue loss (type b) showed variable photophysiological responses (neoplasia and pigmentation response). Only the bleached foci associated with white patch syndrome appeared to impact primarily on the symbiotic dinoflagellates, as evidenced by declines in minimum fluorescence (F0) and maximum quantum yield (Fv/Fm), with no indication of degeneration in the host tissues. Our results suggest that for the majority of coral syndromes from the GBR, pathogenesis occurs in the host tissue, while the impact on the zooxanthellae populations residing in affected corals is minimal.