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Growth anomalies (GAs), one of the diseases recently reported for scleractinian corals, are characterized by an abnormal skeletal structure and reduced zooxanthella density. The pathological characteristics of GAs were studied in colonies of Porites australiensis on a reef in Kayo, Okinawa, Japan. Corallites in the GA region lost the skeletal architecture characteristic of P. australiensis, and polyp density had decreased in the GAs due to enlargement of both calices and the coenosteum. The gross productivity of isolated GA samples was lower than in healthy samples and decreased to almost 0 within 11 d after isolation. However, when GA samples were brought into contact with healthy-looking samples from the same colony, they fused and both the GA and healthy regions grew. Healthy samples fused with GA samples grew more slowly than those fused with healthy samples. For in situ GAs surrounded by healthy tissue, tissue death usually started at the center of the GA, probably due to a deficiency in the translocated energy supply from the surrounding tissue. The total area of the GA region and the dead area increased at a rate of 5.3 ± 2.9 cm 2 yr −1. These results suggest that GA regions are maintained by energy supplies from surrounding healthy tissues and that GAs may have a negative impact on host corals. KEY WORDS: Coral · Disease · Growth anomaly · Porites australiensisResale or republication not permitted without written consent of the publisher

Background: When coral planulae, which use a horizontal mode of symbiont transmission, are inoculated with Symbiodinium, they suffer greater oxidative stress under strong light or high-temperature stress than non-symbiotic counterparts. Thus, dinoflagellate symbionts may become a source of reactive oxygen species (ROS) under stress. However, it remains unknown whether vertically transmitted symbionts negatively affect coral larvae under stress. We investigated the thermal tolerance of symbiotic planulae of a vertical transmitter coral, Pocillopora damicornis. Results: P. damicornis larvae, which have a large number of symbionts, survived the high-temperature treatment (32°C) for 2 weeks. Significant reductions in Symbiodinium cell density were observed, but these did not lead to increased mortality of planulae during the 2-week experimental period. Although no significant difference was detected in the percentage of apoptotic cells between temperature treatment groups, pre-bleaching larvae exposed to 31°C tended to exhibit higher percentages of apoptotic (TUNEL-positive) cells in the gastrodermis than 32°C-treated larvae, which contained reduced numbers of Symbiodinium cells. Conclusions: Symbiotic larvae of P. damicornis survived well under high-temperature conditions, although their Symbiodinium cell density decreased. This suggests that P. damicornis larvae have the capacity to reduce the symbiont cell density without a harmful effect on their survivorship under thermal stress. Further studies on antioxidant systems and possible suppression of apoptotic pathways are necessary to elucidate the mechanism underlying the high thermal tolerance of symbiotic larvae of P. damicornis.

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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 ...