Differential expression and functional diversification of diverse immunoglobulin domain-containing protein (DICP) family in three gynogenetic clones of gibel carp

Differential expression and functional diversification of diverse immunoglobulin domain-containing protein (DICP) family in three gynogenetic clones of gibel carp
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银鲫三个雌核发育克隆中不同免疫球蛋白结构域蛋白(DICP)家族的差异表达和功能多样化

DOI:
10.1016/j.dci.2018.03.013
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发表时间:
2018-07-01
影响因子:
2.9
通讯作者:
Gui, Jian-Fang
Gui, Jian-Fang
中科院分区:
生物学3区
文献类型:
--
作者:
Gao, Fan-Xiang;Lu, Wei-Jia;Gui, Jian-Fang

文献摘要

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含IG结构域蛋白(DICP)家族是一个新的硬骨鱼特异性多基因家族,编码多种免疫受体。然而,它们的功能和结合伴侣的含义仍然未知。本研究首次从银鲫雌核发育的3个克隆中鉴定出28个DICPs,揭示了它们的高度变异性和克隆特异性。鲫鱼疱疹病毒(CaHV)感染后,这些DICPs在头肾、肾脏和脾脏中明显上调。克隆A(+)、F和H的上调倍数与对CaHV的敏感性有关,从抗性克隆到敏感克隆上调倍数逐渐增加。过量表达银鲫DICPs抑制干扰素(IFN)和蝰蛇蛋白启动子驱动的荧光素酶活性。E.大肠杆菌提取物和脂质A显著增强了抑制作用。异育银鲫DICPs与SHP-1和SHP-2有相互作用。这些结果表明,鲤鱼DICPs可能作为抑制性受体,特异性识别脂质A,然后与SHP-1和SHP-2相互作用,抑制IFN和ISGs的诱导。(C)2018由Elsevier Ltd.出版
Diverse immunoglobulin (Ig) domain-containing protein (DICP) family is a novel bony fish-specific multi gene family encoding diversified immune receptors. However, their function and the implication of binding partners remain unknown. In this study, we first identified 28 DICPs from three gibel carp gynogenetic clones and revealed their high variability and clone-specific feature. After crucian carp herpesvirus (CaHV) infection, these DICPs were significantly upregulated in head kidney, kidney and spleen. The up-regulation folds in clone A(+), F and H were related to the susceptibility to CaHV, progressively increasing from resistant clone to susceptible clone. Overexpression of gibel carp DICPs inhibited interferon (IFN) and viperin promoter-driven luciferase activity. The additions of E. coli extracts and lipid A significantly enhanced the inhibition effect. In addition, gibel carp DICPs can interact with SHP-1 and SHP-2. These findings suggest that gible carp DICPs, as inhibitory receptors, might specifically recognize lipid A, and then interact with SHP-1 and SHP-2 to inhibit the induction of IFN and ISGs. (C) 2018 Published by Elsevier Ltd.