Isolation and expression analysis of an MAPKK gene from Fenneropenaeus chinensis in response to white spot syndrome virus infection
文献类型: 外文期刊
作者: Li, Xupeng 1 ; Kong, Jie 1 ; Meng, Xianhong 1 ; Luo, Kun 1 ; Luan, Sheng 1 ; Cao, Baoxiang 1 ; Liu, Ning 1 ;
作者机构: 1.Chinese Acad Fishery Sci, Yellow Sea Fisheries Res Inst, Minist Agr, Key Lab Sustainable Utilizat Marine Fisheries Res, 106 Nanjing Rd, Qingdao 266071, Peoples R China
2.Qingdao Natl Lab Marine Sci & Technol, Lab Marine Fisheries Sci & Food Prod Proc, 1 Wenhai Rd, Qingdao 266300, Peoples R China
关键词: Mitogen-activated protein kinase kinase (MAPKK); Fenneropenaeus chinensis; White spot syndrome virus (WSSV); Expression
期刊名称:FISH & SHELLFISH IMMUNOLOGY ( 影响因子:4.581; 五年影响因子:4.851 )
ISSN: 1050-4648
年卷期: 2016 年 55 卷
页码:
收录情况: SCI
摘要: Mitogen-activated kinase kinase (MAPKK) is an important gene involved in the host-virus interaction process. To obtain a better understanding of MAPKK in the interaction process between the Chinese shrimp Fenneropenaeus chinensis and white spot syndrome virus (WSSV), we cloned the sequence of an MAPKK cDNA fromF. chinensis (FcMAPKK) and investigated the effect of FcMAPKK on WSSV infection. The results showed that the FcMAPICK gene contained a 1227 bp open reading frame (ORF), which encoded a highly conserved protein with a serine/threonine protein kinase catalytic (S_TKc) domain. The deduced amino acid sequence of FcMAPKIC shared identities between 11.9 and 92.6% with MAPKKs from vertebrate, invertebrate, plant and fungus species. The FcMAPKK was expressed in all the examined tissues in the normal F. chinensis. FcMAPKK expression level was highest in the hepatopancreas where it was approximately 2.6-fold the expression level in the gill, and lowest in the muscle where it was approximately 0.3-fold the expression level in the hepatopancreas. The FcMAPKK expression levels in the muscle, gill, and hepatopancreas were all changed post WSSV challenge. The FcMAPKK expression was significantly (P < 0.01) up-regulated in the muscle of F. chinensis at 48 h post WSSV infection. The WSSV began to replicate quickly in the normal F. chinensis at 48 h post infection, while the WSSV replication in the U0126-treated F. chinensis could be significantly (P < 0.05) inhibited. The results suggested that FcMAPKK might be involved in the WSSV infection process, and hijacking of FcMAPKK might be required for WSSV replication in F. chinensis. (C) 2016 Published by Elsevier Ltd.
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