TLR18基因在鲤感染CyHV-3中的表达模式及信号通路  

Expression pattern and related signal pathway of TLR18 in CyHV-3 infection of cyprinid carp

作　　者：任婉莹 姜晓娜 葛彦龙[2] 田立静 李 李池陶[2] 田景文 胡雪松[2] 石潇丹 石连玉[2] 贾智英[1,2] REN Wanying;JIANG Xiaona;GE Yanlong;TIAN Lijing;LI Yan;LI Chitao;TIAN Jingwen;HU Xuesong;SHI Xiaodan;SHI Lianyu;JIA Zhiying(National Demonstration Center for Experimental Fisheries Science Education,Shanghai Ocean University,Shanghai 201306,China;Key Laboratory of Aquatic Genomics,Ministry of Agriculture and Rural Affairs,Heilongjiang River Fisheries Research Institute,Harbin 150070,Heilongjiang,China;Shanghai Collaborative Innovation for Aquatic Animal Genetics and Breeding,Shanghai Ocean University,Shanghai 201306,China)

机构地区：[1]上海海洋大学水产科学国家级实验教学示范中心,上海201306 [2]中国水产科学研究院黑龙江水产研究所农业农村部水产基因组学重点实验室,黑龙江哈尔滨150070 [3]上海海洋大学水产物遗传育种中心上海市协同创新中心,上海201306

出　　处：《上海海洋大学学报》2023年第3期500-509,共10页Journal of Shanghai Ocean University

基　　金：黑龙江省自然科学基金项目(TD2019C004);中国水产科学研究院基本科研业务费资助项目(2020TD31);中央级公益性科研院所基本科研业务费专项(HSY202109Q);国家现代农业产业技术体系项目(CARS-45-06)。

摘　　要：以抗病镜鲤选育系F4和德国镜鲤选育系为实验材料,通过RT-PCR技术确定鲤受CyHV-3感染过程两组鱼脾脏组织中TLR18、接头蛋白MyD88及相应配体TRAF6、下游因子IRF5及P65基因的表达模式,并分析其在抗病镜鲤选育系F4中的相关抗病机制。结果显示:TLR18、MyD88、TRAF6、IRF5基因在两组鱼间均呈先上升后下降并趋于平稳趋势,在48 h达到最高,而P65基因在未选育组呈先上升后下降并恢复初始水平趋势,在48 h达到最高,在选育组呈下降后恢复初始水平趋势。在未感染CyHV-3时,TLR18与IRF5基因相对表达量在选育组极显著低于未选育组,MyD88、TRAF6与P65基因相对表达量在选育组极显著高于未选育组;到CyHV-3感染早期,TLR18与P65基因相对表达量在选育组极显著低于未选育组,MyD88、TRAF6及IRF5基因相对表达量在选育组显著高于未选育组。推测在CyHV-3感染过程中,TLR18基因通过依赖MyD88途径产生IRF5基因清除病毒的同时激活NF-κB信号通路,且选育组较未选育组通过产生较多IRF5基因清除病毒,而未选育组较选育组显著激活NF-κB信号通路产生相关炎症因子,这可能与选育组抗病性及抗病机制有关。该结果不仅验证了选育组在机体基础水平及先天免疫过程中对CyHV-3抗性的增强,还为深入研究选育组抗病机制及鱼类TLRs在病毒感染过程中的作用及其相关信号通路奠定基础。The expression patterns of TLR18,MyD88,and corresponding ligand TRAF6,downstream factor IRF5,and P65 in spleen tissues of breeding strain F 4 and German mirror carp were determined by RT-PCR.The difference of related genes in disease resistance mechanism between breeding strain F 4 and German mirror carp was analyzed.The results show:the expression of TLR18,MyD88,TRAF6,and IRF5 showed the same trend between the two groups,which increased first,then decreased and stabilized,and reached the highest at 48 h,while the relative expression of P65 in non-breeding strain increased first,then decreased and recovered to the initial level,and reached the highest at 48 h.In breeding strain,the expression trend decreased and then recovered to the initial level.The relative expression of TLR18 and IRF5 in breeding strain was significantly lower than that in the non-breeding strain without CyHV-3 infection.The relative expression levels of MyD88,TRAF6,and P65 in breeding strain were significantly higher than those in non-breeding strain.At the early stage of CyHV-3 infection,the relative expression levels of TLR18 and P65 in breeding strain were significantly lower than those in non-breeding strain,while the relative expression levels of MyD88,TRAF6,and IRF5 in breeding strain were significantly higher than those in non-breeding strain.It is speculated that during CyHV-3 infection,TLR18 generateed IRF5 by binding to TRAF6 through the MyD88 pathway,which cleared the virus and activated the NF-κB signaling pathway to produce inflammatory factors.In breeding strain,more IRF5 was produced and the NF-κB signaling pathway was not significantly activated to resist the virus.This result may be related to breeding.These results not only verified the improvement of CyHV-3 resistance in breeding strain in the body basic condition and innate immunity but also laid a foundation for further study of the role of fish TLRs in the process of virus infection and related signaling pathways.

关 键 词：鲤 TLR18 CyHV-3 选育 

分 类 号：S917[农业科学—水产科学]