The categorization and mutual modulation of expanded MyD88s in Crassostrea gigas

MyD88 serves as a critical cytosolic adaptor mediating activation of NF-kappa B in innate immunity. It has been found that there is a considerable expansion of MyD88 in Crassostrea gigas. In the present study, four typical MyD88 genes in Crassostrea gigas (CgMyD88-A to CgMyD88-D) were successfully c...

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Bibliographic Details
Published in:Fish & Shellfish Immunology
Main Authors: Xin, Lusheng, Wang, Mengqiang, Zhang, Huan, Li, Meijia, Wang, Hao, Wang, Lingling, Song, Linsheng
Format: Article in Journal/Newspaper
Language:English
Published: 2016
Subjects:
Crassostrea Gigas
Myd88
Innate Immunity
Death Domain
Tir Domain
Nf-kappa b
Crassostrea gigas
Online Access:http://ir.qdio.ac.cn/handle/337002/130995
https://doi.org/10.1016/j.fsi.2016.04.014
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Summary:MyD88 serves as a critical cytosolic adaptor mediating activation of NF-kappa B in innate immunity. It has been found that there is a considerable expansion of MyD88 in Crassostrea gigas. In the present study, four typical MyD88 genes in Crassostrea gigas (CgMyD88-A to CgMyD88-D) were successfully cloned and their potential functions were investigated together with another two known ones (CgMyD88-T1 and CgMyD88-T2). Multiple alignments revealed that CgMyD88-B and CgMyD88-C remained the conserved DD and TIR domains, while there was a significant variation of E51Q in the DD of CgMyD88-A, and some variations in both DD and TIR domains of CgMyD88-D, respectively. Both truncated CgMyD88-T1 and CgMyD88-T2 lacked Box II in their only TIR domains. Expression pattern analysis showed that CgMyD88-B and CgMyD88-C genes possessed higher expression in normal tissues, compared with the other four. When oysters were under bacteria challenge, CgMyD88-B, CgMyD88-C, CgMyD88-T1 and CgMyD88-T2 were firstly induced, while CgMyD88-A and CgMyD88-D were suppressed. Dual luciferase reporter assays showed that CgMyD88-B and CgMyD88-C could promote the activation of NF-kappa B signaling pathway, while the other four CgMyD88 genes failed or even suppressed the activities of CgMyD88-B and CgMyD88-C on the activation of NF-kappa B signaling. It was deduced that after oysters were challenged by bacteria, CgMyD88-B and CgMyD88-C could rapidly and efficiently activate NF-kappa B signaling pathway to elicit anti-pathogen responses before suppressor CgMyD88 genes (CgMyD88-T1 and CgMyD88-T2) exceeding their expression level. These results suggested that there was mutual modulation of expanded CgMyD88 genes on activating NE-kappa B signaling pathway in oyster C. gigas. (C) 2016 Elsevier Ltd. All rights reserved.

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