Identification, characterization, and function analysis of the NF-κB repressing factor (NKRF) gene from Litopenaeus vannamei

Identification, characterization, and function analysis of the NF-κB repressing factor (NKRF) gene from Litopenaeus vannamei
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凡纳滨对虾 NF-kappaB 抑制因子 (NKRF) 基因的鉴定、表征和功能分析。

DOI:
10.1016/j.dci.2017.05.020
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发表时间:
2017-11-01
影响因子:
2.9
通讯作者:
Xu, Xiaopeng
Xu, Xiaopeng
中科院分区:
生物学3区
文献类型:
--
作者:
Qiu, Wei;He, Jian-hui;Xu, Xiaopeng

文献摘要

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NF-κ B家族转录因子调节广泛的生物过程,特别是免疫应答。在人体中的研究表明,NF-κ B阻遏因子(NKRF)通过直接的蛋白质相互作用负性调节NF-κ B的活性。然而,迄今为止,NKRF的功能尚未在哺乳动物之外进行研究。本研究从太平洋白色凡纳滨对虾(Litopenaeus vannamei)中克隆了一个NKRF基因(LvNKRF),该基因与昆虫、鱼类和哺乳动物的NKRF基因具有同源性。LvNKRF在肠、胃和肌肉组织中高表达,定位于细胞核。LvNKRF可以与虾NF-κ B家族的两个成员Dorsal和Relish相互作用。有趣的是,虽然与人NKRF共享相似的蛋白质结构,但LvNKRF对Dorsal和Relish的活性没有抑制作用,而是增强作用,这与哺乳动物NKRF相反。革兰氏阳性菌、革兰氏阴性菌和免疫刺激剂脂多糖(LPS)、poly(I:C)均不能诱导LvNKRF的表达,但白色斑点综合征病毒(WSSV)感染后LvNKRF的表达显著上调。LvNKRF基因的沉默显著降低了WSSV感染引起的对虾死亡率,并下调了WSSV在各组织中的拷贝数和WSSV结构基因的表达。这表明LvNKRF可以促进WSSV感染对虾,这可能是WSSV劫持热NF-κ B途径以利于自身复制的另一种策略。本研究为进一步研究NKRFs的进化起源提供了有价值的背景,并为无脊椎动物NF-κ B通路调控机制的研究提供了便利。(C)2017爱思唯尔有限公司版权所有
The NF-kappa B family transcription factors regulate a wide spectrum of biological processes, in particular immune responses. The studies in human suggest that the NF-kappa B repressing factor (NKRF) negatively regulates the activity of NF-kappa B through a direct protein protein interaction. However, the function of NKRF has not been studied outside mammals up to now. The current study identified a NKRF gene (LvNKRF) from the Pacific white shrimp, Litopenaeus vannamei, which showed homology with NKRFs from insects, fishes and mammals. LvNKRF was high expressed in intestine, stomach and muscle tissues and was localized in the nucleus. LvNKRF could interact with both Dorsal and Relish, the two members of the shrimp NF-kappa B family. Interestingly, although sharing a similar protein structure with that of human NKRF, LvNKRF showed no inhibitory but instead enhancing effects on activities of Dorsal and Relish, which was contrary to those of mammalian NKRFs. The expression of LvNKRF could not be induced by Gram-positive and-negative bacteria and immunostimulants lipopolysaccharide (LPS) and poly (I:C) but was significantly up-regulated after white spot syndrome virus (WSSV) infection. Silencing of LvNKRF significantly decreased the mortalities of shrimp caused by WSSV infection and down-regulated the WSSV copies and the expression of WSSV structural gene in tissues. These suggested that LvNKRF could facilitate the infection of shrimp by WSSV, which may be an additional strategy for WSSV to hijack the hot NF-kappa B pathway to favor its own replication. The current study could provide a valuable context for further investigating the-evolutionary derivation of NKRFs and facilitate the study of regulatory mechanisms of invertebrate NF-kappa B pathways. (C) 2017 Elsevier Ltd. All rights reserved.