Involvement of eIF2 alpha of Epinephelus coioides in the fish immune response to virus infection
Involvement of eIF2 alpha of Epinephelus coioides in the fish immune response to virus infection
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斜带石斑鱼 eIF2 α 参与鱼对病毒感染的免疫反应
DOI：
10.1016/j.fsi.2018.02.027
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发表时间：
2018
影响因子：
4.7
通讯作者：
Qin Qiwei
中科院分区：
文献类型：
--
作者：
Zang Shaoqing;Zhang Xin;Zhang Jingcheng;Li Chen;Wei Jingguang;Qin Qiwei
真核细胞起始因子2α亚基(eIF2α)是一种关键的翻译调节因子，在包括病毒感染在内的不同细胞压力和刺激下发挥重要作用。本研究克隆了斜带石斑鱼eif2α同源基因(α)，并对其在鱼类病毒感染中的作用进行了研究。EceIF2α编码315个氨基酸残基，与其他物种的αS有很高的相似性。实时定量聚合酶链式反应分析表明，EceIF2α在所有受检组织中均有分布。EceIF2α在小鼠脾和头肾组织中的表达水平。当用多聚肌苷-多胞苷(Poly[I：C])激发时，类碘的表达上调。石斑鱼脾(GS)细胞中EceIF2α大量分布于胞浆和胞核。EceIF2α的过表达提高了赤点石斑鱼神经坏死病毒基因在GS细胞中的表达。此外，EceIF2α还可抑制NK-κB和β的激活。此外，去磷酸化抑制剂处理导致RGNNV基因转录显著降低。综上所述，这些结果提示EceIF2α可能参与了鱼类对病毒攻击的免疫应答。
The eukaryotic initiation factor 2 alpha subunit (eIF2α) is a key translation regulator that plays an important role in different cellular pressures and stimuli, including virus infection. In the present study, an eIF2α homolog (EceIF2α) from the orange-spotted grouper (Epinephelus coioides) was cloned and its roles during fish viral infection were characterized. EceIF2α encodes a putative protein of 315 amino acid residues, and shares a high degree of similarity with eIF2αs from other species. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis indicated that EceIF2α was distributed in all examined tissues. Both of the expression levels of EceIF2α in the spleen and head kidney ofE. coioideswere up-regulated when challenged with polyinosine-polycytidylic acid (poly[I:C]). EceIF2α was abundantly distributed in both the cytoplasm and nucleus in grouper spleen (GS) cells. Over-expression of EceIF2α improved the expression of red-spotted grouper nervous necrosis virus (RGNNV) genes in GS cells. In addition, EceIF2α depressed the activation of NK-κB and IFN-β. Furthermore, dephosphorylation inhibitor treatment led to a significant decrease of RGNNV gene transcription. Taken together, these results suggest that EceIF2α might be involved in the fish immune response to virus challenge.