Characterisation of RelA and RelB in spotted sea bass (Lateolabrax maculatus): RelA and RelB can be activated by peptidoglycan

文献类型： 外文期刊

第一作者： Liu, Danjie

作者： Liu, Danjie;Sun, Zhaosheng;Yuan, Shuya;Cai, Chuanguo;Liu, Qigen;Gao, Qian;Liu, Danjie;Sun, Zhaosheng;Yuan, Shuya;Cai, Chuanguo;Liu, Qigen;Gao, Qian;Zhou, Zhigang

作者机构：

关键词： NF-kappa B; RelA and RelB; Innate immunity; PGRP; Lateolabrax maculatus

期刊名称：AQUACULTURE （ 影响因子：3.9； 五年影响因子：4.4 ）

ISSN： 0044-8486

年卷期： 2025 年 603 卷

页码：

收录情况： SCI

摘要： NF-kappa Bs, including RelA (p65), RelB, C-Rel, NF-kappa B1 (p105/p50) and NF-kappa B2 (p100/p52), are transcription factors that control DNA transcription and play an important role in the inflammatory response. In this study, two NF-kappa B genes of spotted sea bass (Lateolabrax maculatus), LmRelA and LmRelB, were cloned and characterized. Multiple sequence alignment showed that LmRelA and LmRelB were conserved with Rel-homology domain (RHD) and IPT domains. Additionally, the identified LmRelA and LmRelB were widely distributed in various tissues of the spotted sea bass. After stimulation with LPS, Poly (I: C) and Edwardsiella tarda in the immune tissues and with peptidoglycan (PGN) in primary head kidney cells, the LmRelA and LmRelB were significantly up-regulated, indicating that the LmNF-kappa B might play a role in the defense against bacteria and/or virus invasion. Analysis of the LmRelA and LmRelB promoters revealed that there were many transcription factors binding sites on the promoters, including NF-kappa B itself and AP-1. In addition, dual-luciferase reporter gene assays for LmRelA and LmRelB promoters showed that LPS and PGN induced the transcription of both genes. Subcellular localization assay of LmRelA and LmRelB indicated that they were activated and entered the nuclei from the cytoplasm after the stimulation with PGN. Interestingly, the overexpression of PGRP-SC2 of spotted sea bass (LmPGRP-SC2) promoted the activation of LmRelA during PGN stimulation but inhibited the expression of LmRelB, suggesting that PGN might induce the transcription of LmRelA through PGRP-SC2, but induction of LmRelB does not depend on PGRP-SC2. Overall, our results demonstrated that LmRelA and LmRelB were activated by PGN stimulation and then entered the nucleus, and the activation response were affected by PGRP-SC2.

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