Growth anomalies (GAs) in corals are characterized by morphological abnormalities of the skeleton as well as polyps and coenosarcs. GAs commonly appear as protuberances with fewer polyps and are paler in color due to decreased zooxanthellae density. To test the hypothesis that morphological anomalies in GAs may be caused by unregulated cellular kinetics, the relative abundances of apoptotic cells and proliferating cells were compared between GAs and apparently healthy regions in 2 corals, Porites australiensis and Montipora informis. Apoptotic cells and proliferating cells were detected using TUNEL assays and BrdU incorporation assays, respectively. The labeling indices for apoptotic nuclei and BrdU-labeled nuclei were measured in the epidermis, oral gastrodermis, aboral gastrodermis, and calicodermis. The labeling index for apoptotic nuclei in the oral gastrodermis and the calicodermis was significantly lower in GAs than in healthy regions in both coral species. The index for BrdU-labeled cells in the calicodermis was significantly higher in GAs than in healthy regions in both coral species. When GA regions partially died, the GA tissues directly adjacent to the dead areas exhibited signs of necrosis, although some apoptotic cells were also present. Healthy oral gastrodermis adjacent to the border between the healthy and GA regions exhibited higher frequencies of apoptotic cells. These results suggest that apoptotic pathways were suppressed and cell proliferation was promoted in GA regions, although cells in GAs may die through both necrosis and apoptosis.
KEY WORDS: Apoptosis · Necrosis · Cell proliferation · Coral disease · Growth anomaly · Porites australiensis · Montipora informis
Resale or republication not permitted without written consent of the publisherDis Aquat Org 102: [1][2][3][4][5][6][7][8][9][10][11] 2012 MutY, Hsp90a1, GRP75, and metallo thionein, which are hyperplasia-associated proteins, were upregulated in GAs in Porites compressa. Their results also indicate hyper-proliferation of cells in GA tissues. However, the mechanism and the process of cellular kinetics in GA regions are not yet understood.The etiology of GA is still unclear, although relationships between GA prevalence and several factors have been suggested, including UVB radiation (Peters et al. 1986, Coles & Seapy 1998, nutrients and organic carbon (Kaczmarsky & Richardson 2010), water temperatures and photosynthetically active radiation (Stimson 2010), water turbidity and depth (Williams et al. 2010), host density and human population size , and aging (Irikawa et al. 2011). GA regions are frequently associated with microorganisms in the tissue as well as skeletal space (Coles & Seapy 1998, Work & Rameyer 2005, Work et al. 2008, and the microorganisms have been suggested to be involved in GAs (Work & Rameyer 2005, Domart-Coulon et al. 2006). However, microorganisms are not always detected in GAs (Yamashiro et al. 2000, and the linkages between their presence and GA development are currently unknown.GA-affected corals ...