Molecular characterization, expression and functional analysis of IRAK1 and, Cheek for IRAK4 in Nile tilapia (Oreochromis niloticus)
文献类型： 外文期刊
作者： Han, Xueqing 1 ; Gao, Fengying 1 ; Lu, Maixin 1 ; Liu, Zhigang 1 ; Wang, Miao 1 ; Ke, Xiaoli 1 ; Yi, Mengmeng 1 ; Cao, Ji 1 ;
作者机构： 1.Chinese Acad Fishery Sci, Pearl River Fisheries Res Inst, 1 Xing Yu Rd, Guangzhou 510380, Guangdong, Peoples R China
2.Minist Agr, Key Lab Trop & Subtrop Fishery Resource Applicat, Beijing, Peoples R China
3.Shanghai Ocean Univ, Natl Demonstrat Ctr Expt Fisheries Sci Educ, Shanghai 201306, Peoples R China
关键词： Nile tilapia (Oreochromis niloticus); IRAK1; IRAK4; Immune response; Expression; NF-kappa B activation
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： 2020 年 97 卷
页码：
收录情况： SCI
摘要： Interleukin-1 receptor-associated kinase 1 (IRAK1) and IRAK4 are critical signalling mediators and play pivotal roles in the innate immune and inflammatory responses mediated by TLR/IL-1R. In the present study, two IRAK family members, OnIRAK1 and OnIRAK4, were identified in the Nile tilapia Oreochromis niloticus with a conserved N-terminal death domain and a protein kinase domain, similar to those of other fishes and mammals. The gene structures of OnIRAK1 and OnIRAK4 are organized into fifteen exons split by fourteen introns and ten exons split by nine introns. OnIRAK1 and OnIRAK4 were broadly expressed in all of the tissues tested, with the highest expression levels being observed in the blood and the lowest expression levels being observed in the liver. Both genes could be detected from 2 d post-fertilization (dpf) to 8 dpf during embryonic development. Moreover, the expression levels of OnIRAK1 and OnIRAK4 were clearly altered in all five tissues after Streptococcus agalactiae infection in vivo and could be induced by LPS, Poly I: C, S. agalactiae WC1535 and Delta CPS in Nile tilapia macrophages. The overexpression of OnIRAK1 and OnIRAK4 in 293T cells showed that they were both distributed in the cytoplasm and could significantly increase NF-kappa B activation. Interestingly, after transfection, OnIRAK1 significantly upregulated OnMyd88-induced NF-kappa B activation, while OnIRAK4 had no effect on OnMyd88-induced NF-kappa B. activation. Co-immunoprecipitation (Co-IP) assays showed that OnMyd88 did not interact with either OnIRAK1 or OnIRAK4 and that OnIRAK1 did not interact with OnIRAK4. Taken together, these findings suggest that OnIRAK1 and OnIRAK4 could play important roles in TLR/IL-1R signalling pathways and the immune response to pathogen invasion.
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