Richardson Laurie L, Miller Aaron W, Broderick Emily, Kaczmarsky Longin, Gantar Miroslav, Stanić Dina, Sekar Raju
Department of Biological Sciences, Florida International University, Miami, Florida 33199, USA.
Dis Aquat Organ. 2009 Nov 16;87(1-2):79-90. doi: 10.3354/dao02083.
Black band disease (BBD) consists of a cyanobacterial-dominated, sulfide-rich microbial mat that migrates across coral colonies, degrading coral tissue. The mat contains diverse bacteria that include photoautotrophs (cyanobacteria), sulfate-reducers, sulfide-oxidizers, and organoheterotrophs. BBD sulfate-reducers contribute to BBD pathobiology by production of sulfide, which causes coral tissue lysis and death, and the cyanotoxin microcystin is produced by BBD cyanobacteria. Here we used a model system of coral fragments to investigate the roles of sulfide and microcystin in BBD by exposure to the metabolic inhibitors sodium molybdate and 3-(3', 4'-dichlorophenyl)-1, 1-dimethylurea (DCMU), which inhibit sulfate reduction and oxygenic photosynthesis, respectively. Exposure of BBD inocula to sodium molybdate prior to inoculation prevented infection of healthy fragments but did not prevent continued band migration and coral tissue lysis by active BBD infections. Exposure to DCMU did not inhibit either the initiation of BBD or continued migration of active BBD. Exposure of healthy coral fragments to sulfide, purified microcystin, and a combination of both revealed that both microcystin and sulfide are toxic to coral and act synergistically. Measurement of growth of bacteria isolated from BBD and the healthy coral surface mucopolysaccharide layer (SML) during exposure to microcystin revealed that growth of relatively more BBD than SML isolates was stimulated, although effects were not uniform and the majority exhibited no effect. Our results indicate that sulfide is required for initiation of BBD, both microcystin and sulfide are involved in BBD pathobiology, and microcystin may structure the BBD bacterial community.
黑带病（BBD）由以蓝藻为主、富含硫化物的微生物席组成，该微生物席会在珊瑚群体上移动，降解珊瑚组织。这种微生物席包含多种细菌，包括光合自养生物（蓝藻）、硫酸盐还原菌、硫化物氧化菌和有机异养菌。BBD硫酸盐还原菌通过产生硫化物促进黑带病的病理生物学过程，硫化物会导致珊瑚组织溶解和死亡，并且BBD蓝藻会产生蓝藻毒素微囊藻毒素。在此，我们使用珊瑚碎片模型系统，通过暴露于代谢抑制剂钼酸钠和3-（3'，4'-二氯苯基）-1，1-二甲基脲（DCMU）来研究硫化物和微囊藻毒素在黑带病中的作用，这两种抑制剂分别抑制硫酸盐还原和氧光合作用。在接种前将BBD接种物暴露于钼酸钠可防止健康碎片受到感染，但无法阻止活跃的BBD感染导致的条带持续迁移和珊瑚组织溶解。暴露于DCMU既不抑制BBD的起始，也不抑制活跃BBD的持续迁移。将健康的珊瑚碎片暴露于硫化物、纯化的微囊藻毒素以及两者的组合中发现，微囊藻毒素和硫化物对珊瑚都有毒性，且具有协同作用。在暴露于微囊藻毒素期间，对从BBD和健康珊瑚表面黏液多糖层（SML）分离出的细菌的生长进行测量发现，虽然效果并不一致且大多数没有表现出影响，但受到刺激的BBD分离株相对比SML分离株更多。我们的结果表明，硫化物是黑带病起始所必需的，微囊藻毒素和硫化物都参与了黑带病的病理生物学过程，并且微囊藻毒素可能会影响黑带病细菌群落的结构。
