Transcriptomic profiles of striped snakehead fish cells (SSN-1) infected with red-spotted grouper nervous necrosis virus (RGNNV) with an emphasis on apoptosis pathway
Transcriptomic profiles of striped snakehead fish cells (SSN-1) infected with red-spotted grouper nervous necrosis virus (RGNNV) with an emphasis on apoptosis pathway
复制标题
感染红点石斑鱼神经坏死病毒（RGNNV）的条纹蛇头鱼细胞（SSN-1）的转录组谱，重点关注凋亡途径
DOI：
10.1016/j.fsi.2016.11.059
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发表时间：
2017-01-01
影响因子：
4.7
通讯作者：
Lin, Li
中科院分区：
文献类型：
--
作者：
Chen, Wenjie;Yi, Lizhu;Lin, Li
神经坏死病毒（Nervous Necrosis Virus，NNV）是病毒性神经坏死病（viral nervous necrosis disease，VNN）的病原体，在世界范围内引起海水和淡水养殖鱼类的大量死亡，给水产养殖业造成巨大的经济损失。然而，NNV致病性的分子机制仍然知之甚少。本研究利用深度RNA测序技术研究了赤点石斑鱼NNV（RGNNV）感染黑线鳢（Channa striatus）细胞（SSN-1）后转录组的变化。从254，955，234个原始读段中，获得总共253，338，544个干净读段，并将它们组装成93，372个单基因。从RGNNV感染或模拟感染的SSN-1细胞中鉴定出差异表达基因（DEG），包括在感染后3 h（h）分别上调1184个和下调1456个基因，以及在感染后24 h分别上调1138个和下调2073个基因。这些DEG参与了多种与病毒致病相关的信号通路，包括视黄酸诱导基因I（RIG-I）样受体通路、凋亡通路、氧化磷酸化、PI3K-Akt信号通路和MAPK信号通路。随后对细胞凋亡途径的分析表明，内切酶G（EndoG）的表达上调后，RGNNV感染后3和24小时poi。因此，我们克隆了EndoG基因，并对其功能进行了进一步的研究。结果表明，EndoG过表达也可诱导SSN-1细胞凋亡，提示RGNNV感染可能通过EndoG相关的线粒体途径诱导SSN-1细胞凋亡。这些结果将为NNV的发病机制提供新的线索。(C)2016爱思唯尔有限公司版权所有
Nervous necrosis virus (NNV), the causative agent of viral nervous necrosis (VNN) disease, has caused mass mortality of cultured marine and freshwater fish worldwide, resulting in enormous economic losses in the aquaculture industry. However, the molecular mechanisms underlying the pathogenicity of NNV are still poorly understood. In this study, the transcriptomic profiles of striped snakehead fish (Channa striatus) cells (SSN-1) infected with red-spotted grouper NNV (RGNNV) were investigated using deep RNA sequencing technique. From 254,955,234 raw reads, a total of 253,338,544 clean reads were obtained and they were assembled into 93,372 unigenes. Differentially expressed genes (DEGs) were identified from RGNNV-infected or mock-infected SSN-1 cells, including 1184 up-regulated and 1456 down-regulated genes at 3 h (h) post of infection (poi), and 1138 up-regulated and 2073 down-regulated genes at 24 h poi, respectively. These DEGs were involved in many pathways related to viral pathogenesis, including retinoic acid-inducible gene I (RIG-I) like receptors pathway, apoptosis pathway, oxidative phosphorylation, PI3K-Akt signaling pathway, and MAPK signaling pathway. Subsequent analysis focusing on the apoptosis pathway showed that the expression of Endonuclease G (EndoG) was up-regulated upon RGNNV infection at both 3 and 24 h poi. Therefore, EndoG gene was cloned and its function was further characterized. The results showed that over-expression of EndoG could also induce cellular apoptosis in SSN-1 cells, indicating that RGNNV infection might induce apoptosis of SSN-1 cells via EndoG-associated mitochondrial pathway. These results will shed a new light on the pathogenesis of NNV. (C) 2016 Elsevier Ltd. All rights reserved.