Deubiquitinase cylindromatosis (CYLD) inhibits MAPK and NF-κB activation pathways by deubiquitinating upstream regulatory factors. Although CYLD has been identified and actively studied in mammals, nothing is known about its putative function in fish. In this study, we identified the gene encoding CYLD (OmCYLD) from rainbow trout, Oncorhynchus mykiss, and examined its role during pathogenic infections. The deduced amino acid sequence of OmCYLD contains conserved CAP-Gly and USP domains. In RTH-149 cells, the expression of OmCYLD was increased by stimulation with Edwardsiella tarda and Streptococcus iniae. Gain-of-function and loss-of-function experiments showed that OmCYLD down-regulates the activation of MAPK and NF-κB and the expression of pro-inflammatory cytokines in E. tarda-stimulated RTH-149 cells. These findings suggest that OmCYLD might function like those of mammals to negatively regulate bacteria-triggered signaling pathway in fish.

中文翻译：

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虹鳟Onkihynchus mykiss中去泛素酶CYLD的分子克隆和功能分析。

去泛素化酶圆柱化病（CYLD）通过去泛素化上游调节因子来抑制MAPK和NF-κB活化途径。尽管已经在哺乳动物中发现并积极地研究了CYLD，但对它在鱼类中的假定功能一无所知。在这项研究中，我们从虹鳟Oncorhynchus mykiss中鉴定了编码CYLD（OmCYLD）的基因，并检查了其在致病性感染中的作用。推导的OmCYLD氨基酸序列包含保守的CAP-Gly和USP结构域。在RTH-149细胞中，通过用爱德华氏菌和猪链球菌刺激，OmCYLD的表达增加。功能获得和功能丧失实验表明，OmCYLD下调了受大肠杆菌刺激的RTH-149细胞中MAPK和NF-κB的激活以及促炎性细胞因子的表达。