Tumor formation on the coral Montipora informis

Yamashiro, Hideyuki; Yamamoto, Maria Emília; Woesik, Robert van

doi:10.3354/dao041211

Cited by 60 publications

(72 citation statements)

References 7 publications

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“…The fact that GAs increase in number on an infected individual over time, combined with their lack of normal polyp structure, reduced density of zooxanthellae and lack of digestive organs ) means that they negatively impact affected corals at Palmyra, particularly Acropora and Montipora species. Coral GAs are now widely acknowledged as a deleterious condition, capable of leading to reduced colony growth, decreased density of coral skeleton, loss of mucus secretory cells and nematocysts, reduced density of zooxanthellae, reduced fecundity, tissue necrosis, and a loss, reduction or degeneration of normal polyp structure (Cheney 1975, Bak 1983, Peters et al 1986, Coles & Seapy 1998, Yamashiro et al 2000, Gateno et al 2003, Domart-Coulon et al 2006, Work et al 2008.…”

Section: Disease Severity Fate and Temporal Patternsmentioning

confidence: 99%

Spatial and temporal patterns of scleractinian coral, soft coral, and zoanthid disease on a remote, near-pristine coral reef (Palmyra Atoll, central Pacific)

Williams¹,

Knapp²,

Aeby³

et al. 2011

Dis. Aquat. Org.

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Section: Disease Severity Fate and Temporal Patternsmentioning

confidence: 99%

Spatial and temporal patterns of scleractinian coral, soft coral, and zoanthid disease on a remote, near-pristine coral reef (Palmyra Atoll, central Pacific)

Williams¹,

Knapp²,

Aeby³

et al. 2011

Dis. Aquat. Org.

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“…Over the last 30 yr, coral diseases have been responsible for significant mortalities and coral community structure changes in many Caribbean and Indo-Pacific tropical coral reefs (Gladfelter 1982, Willis et al 2004, Miller et al 2006. Only a few of the common damaging coral diseases of the tropics have been reported from the northern-and southernmost coral reef communities in both the Atlantic−Caribbean (Weil et al 2002, Weil 2004, Francini-Filho et al 2008, and the Indo-Pacific (Yamashiro et al 2000, Yamashiro 2004, Irikawa 2006, Irikawa et al 2011, Dalton & Smith 2006.…”

Section: Introductionmentioning

confidence: 99%

“…Since then, bleaching has been a recurrent event on many reefs (Nakano 2004). Growth anomalies (GA) affecting several species of tabulate Acropora, Porites and Montipora were the first reported coral diseases potentially caused by biotic factors (Yamashiro et al 2000, Irikawa 2006, Irikawa et al 2011) (see Table 1). A condition called Porites pink block disease (PPBD) was later reported to be expanding around the Ryukyu archipelago (Yamashiro 2004), and was attributed to a trematode similar to the one described for massive Porites (trematodiasis) in Hawaii (Aeby 1998).…”

Section: Introductionmentioning

confidence: 99%

Extended geographic distribution of several Indo-Pacific coral reef diseases

Weil¹,

Irikawa²,

Casareto³

et al. 2012

Dis. Aquat. Org.

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Other than coral bleaching, few coral diseases or diseases of other reef organisms have been reported from Japan. This is the first report of lesions similar to Porites ulcerative white spots (PUWS), brown band disease (BrB), pigmentation response (PR), and crustose coralline white syndrome (CCWS) for this region. To assess the health status and disease prevalence, qualitative and quantitative surveys (3 belt transects of 100 m 2 each on each reef) were performed in March and September 2010 on 2 reefs of the Ginowan-Ooyama reef complex off Okinawa, and 2 protected reefs off Zamani Island, in the Kerama Islands 40 km west of Okinawa. Overall, mean (± SD) disease prevalence was higher in Ginowan-Ooyama (9.7 ± 7.9%) compared to Zamami (3.6 ± 4.6%). Porites lutea was most affected by PUWS at Ooyama (23.1 ± 10.4 vs. 4.5 ± 5.2%). White syndrome (WS) mostly affected Acropora cytherea (12. 5 ± 18.0%) in Zamami and Oxipora lacera (10.2 ± 10%) in Ooyama. Growth anomalies (GA) and BrB were only observed on A. cytherea (8.3 ± 6.2%) and A. nobilis (0.8%) at Zamami. Black band disease affected Pachyseris speciosa (6.0 ± 4.6%) in Ooyama only. Pigmentation responses (PR) were common in massive Porites in both localities (2.6 ± 1.9 and 5.6 ± 2.3% respectively). Crustose coralline white syndrome (CCWS) was observed in both localities. These results significantly expand the geographic distribution of PUWS, BrB, PR and CCWS in the Indo-Pacific, indicating that the northernmost coral reefs in the western Pacific are susceptible to a larger number of coral diseases than previously thought.

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“…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 show deteriorated physiological states, such as low fecundity in Montipora spp. (Yamashiro et al 2000, Acropora spp.…”

mentioning

confidence: 99%

“…However, microorganisms are not always detected in GAs (Yamashiro et al 2000, and the linkages between their presence and GA development are currently unknown.…”

mentioning

confidence: 99%

Cellular kinetics in growth anomalies of the scleractinian corals Porites australiensis and Montipora informis

Yasuda¹,

Hidaka²

2012

Dis. Aquat. Org.

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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 ...

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Tumor formation on the coral Montipora informis

Cited by 60 publications

References 7 publications

Spatial and temporal patterns of scleractinian coral, soft coral, and zoanthid disease on a remote, near-pristine coral reef (Palmyra Atoll, central Pacific)

Spatial and temporal patterns of scleractinian coral, soft coral, and zoanthid disease on a remote, near-pristine coral reef (Palmyra Atoll, central Pacific)

Extended geographic distribution of several Indo-Pacific coral reef diseases

Cellular kinetics in growth anomalies of the scleractinian corals Porites australiensis and Montipora informis

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