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热休克蛋白 60 在应对骨骼侵蚀带疾病时的上调,而不是由藻类过度生长引起的,在石珊瑚 Acropora muricata 中。

Up-regulation of Hsp60 in response to skeleton eroding band disease but not by algal overgrowth in the scleractinian coral Acropora muricata.

机构信息

Department of Biotechnologies and Biosciences, University of Milan-Bicocca, Piazza della Scienza 2, 20126 Milan, Italy.

出版信息

Mar Environ Res. 2012 Jul;78:34-9. doi: 10.1016/j.marenvres.2012.03.008. Epub 2012 Apr 14.

Abstract

Heat shock proteins are biomarkers commonly used to determine the effects of abiotic stresses on the physiology of reef building corals. In this study the effectiveness of the Hsp60 as indicator of biotic stresses in the scleractinian coral Acropora muricata was analyzed, considering the whole holobiont. We focused on two biological interactions recognized to be important contributors to coral reef degradation such as a coral disease, the Skeleton eroding band (SEB) caused by the protozoan Halofolliculina corallasia and the algal overgrowth. In the lagoon of Magoodhoo Island (Maldives) fragments of living tissue of A. muricata exposed to these biotic factors were sampled and proteins subjected to Western analysis. The two different biological interactions trigger diverse responses on Hsp60 level. No detectable effect on Hsp60 modulation appeared in colonies subjected to algal overgrowth. On the contrary, corals displayed a robust up-regulation of Hsp60 in the fragments sampled just above the SEB dark band, where the level of Hsp60 was almost twice compared to the control colonies, indicating that the aggressive behavior of the protozoan causes cellular damage also in coral portions neighboring and along the advancing front of the infection. Portions of coral sampled distant to the SEB band showed a Hsp60 level comparable to that observed in healthy colonies. We propose Hsp60 expression as a promising tool to evaluate physiological stress caused by SEB disease in reef corals.

摘要

热休克蛋白是一种常用的生物标志物,用于确定非生物胁迫对造礁珊瑚生理的影响。在这项研究中,分析了热休克蛋白 60(Hsp60)作为指示生物胁迫的指标在石珊瑚 Acropora muricata 中的有效性,考虑到整个共生体。我们专注于两种被认为是珊瑚礁退化的重要因素的生物相互作用,如珊瑚疾病——由原生动物 Halofolliculina corallasia 引起的骨骼侵蚀带(SEB)和藻类过度生长。在马尔代夫马古度胡岛的泻湖,采集了暴露于这些生物因素的活体组织片段,并进行了 Western 分析。两种不同的生物相互作用在 Hsp60 水平上引发了不同的反应。藻类过度生长对 Hsp60 调节没有明显影响。相反,在 SEB 暗带上方采样的珊瑚碎片中,Hsp60 表达水平显著上调,与对照珊瑚相比,Hsp60 的水平几乎增加了一倍,这表明原生动物的侵袭行为也会导致珊瑚邻近和沿感染前沿的细胞损伤。远离 SEB 带采样的珊瑚部分显示出与健康珊瑚中观察到的 Hsp60 水平相当。我们提出 Hsp60 表达作为评估 SEB 疾病对珊瑚礁生理应激的有前途的工具。

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