title: The categorization and mutual modulation of expanded MyD88s in Crassostrea gigas.
abstract: MyD88 serves as a critical cytosolic adaptor mediating activation of NF-κB 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-κB 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-κB signaling. It was deduced that after oysters were challenged by bacteria, CgMyD88-B and CgMyD88-C could rapidly and efficiently activate NF-κB 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 NF-κB signaling pathway in oyster C. gigas.
authors.affiliation: Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China; University of Chinese Academy of Sciences, Beijing 100049, China.
authors.forename: Lusheng
authors.initials: L
authors.lastname: Xin
authors.affiliation: Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China.
authors.forename: Mengqiang
authors.initials: M
authors.lastname: Wang
authors.affiliation: Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China.
authors.forename: Huan
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China; University of Chinese Academy of Sciences, Beijing 100049, China.
authors.forename: Meijia
authors.initials: M
authors.lastname: Li
authors.affiliation: Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China.
authors.forename: Hao
authors.initials: H
authors.lastname: Wang
authors.affiliation: Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China.
authors.forename: Lingling
authors.initials: L
authors.lastname: Wang
authors.affiliation: Key Laboratory of Mariculture & Stock Enhancement in North China's Sea, Ministry of Agriculture, Dalian Ocean University, Dalian 116023, China. Electronic address: lshsong@ms.qdio.ac.cn.
authors.forename: Linsheng
authors.initials: L
authors.lastname: Song
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D049896:Crassostrea / Q000235:genetics* / Q000276:immunology* / Q000378:metabolism; D005786:Gene Expression Regulation; D007113:Immunity, Innate; D053594:Myeloid Differentiation Factor 88 / Q000737:chemistry / Q000235:genetics* / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D010802:Phylogeny; D016415:Sequence Alignment; D015398:Signal Transduction; D014733:Vibrio / Q000502:physiology
chemical_list: D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B
keywords: Crassostrea gigas; Death domain; Innate immunity; MyD88; NF-κB; TIR domain