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太平洋牡蛎中 CgMyD88-1 和 CgMyD88-2 之间的功能关系。

Functional relationship between CgMyD88-1 and CgMyD88-2 in the Pacific oyster.

机构信息

CAS Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, Shandong, 266071, China; Department of Biological Sciences and Biotechnology, Minnan Normal University, Zhangzhou, Fujian, 363000, China.

CAS Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, Shandong, 266071, China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao, Shandong, 266071, China; National & Local Joint Engineering Laboratory of Ecological Mariculture, Qingdao, Shandong, 266071, China.

出版信息

Fish Shellfish Immunol. 2020 Jan;96:138-140. doi: 10.1016/j.fsi.2019.10.060. Epub 2019 Oct 30.

DOI:10.1016/j.fsi.2019.10.060
PMID:31676429
Abstract

MyD88 is a universal adapter protein for the Toll-like receptor/interleukin-1 receptor (TLR/IL-1R) signaling pathway. Since invertebrates are believed to lack MyD88-independent pathways, MyD88 appears more critical in oyster TLR signaling pathway. In the Pacific oyster (Crassostrea gigas), two complete paralogues, named as CgMyD88-1 and CgMyD88-2, have been identified. In the current study, we indicated that CgMyD88-1 and CgMyD88-2 might act synergistically to increase the efficiency of immune signaling by activating NF-κB transcription factor. However, we found that upon stimulation with lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid [poly (I:C)], CgMyD88-1 and CgMyD88-2 show differences in their response: CgMyD88-1 accumulated as large spots in the cytoplasm, while CgMyD88-2 assembled in the cytoplasm and in the membrane. Our results support the theory that expansion of these immune genes is associated with functional diversity.

摘要

MyD88 是 Toll 样受体/白细胞介素-1 受体 (TLR/IL-1R) 信号通路的通用衔接蛋白。由于无脊椎动物被认为缺乏 MyD88 非依赖性途径,因此 MyD88 在牡蛎 TLR 信号通路中似乎更为关键。在太平洋牡蛎 (Crassostrea gigas) 中,已经鉴定出两个完整的同源物,分别命名为 CgMyD88-1 和 CgMyD88-2。在本研究中,我们表明 CgMyD88-1 和 CgMyD88-2 可能通过激活 NF-κB 转录因子协同作用,提高免疫信号的效率。然而,我们发现,在受到脂多糖 (LPS) 或聚肌苷酸:聚胞苷酸 [poly (I:C)] 刺激时,CgMyD88-1 和 CgMyD88-2 在反应上存在差异:CgMyD88-1 在细胞质中积累成大斑点,而 CgMyD88-2 在细胞质和膜中组装。我们的结果支持这样一种理论,即这些免疫基因的扩张与功能多样性有关。

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