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Zebrafish FGFR3 is a negative regulator of RLR pathway to decrease IFN expression.

Abstract

Fibroblast growth factor receptor (FGFR) 3 is one of the four distinct membrane-spanning tyrosine kinases required for proper skeletal development. In fish, the role of FGFR3 is still unclear. In this article, we reveal that zebrafish FGFR3 is a negative regulator of interferon (IFN) production in the innate immune response by suppressing the activity of TANK-binding kinase 1 (TBK1) in the process of virus infection. qPCR experiments demonstrate that the transcriptional level of cellular FGFR3 was upregulated by infection with spring viremia of carp virus (SVCV), indicating that FGFR3 might be involved in the process of host cell response to viral infection. Then, overexpression of FGFR3 significantly impeded the IFN promoter activity induced by a stimulator. In addition, the capabilities of a retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) system to activate IFN promoter were decreased during the overexpression of FGFR3. Subsequently, FGFR3 decreased the phosphorylation of interferon regulatory factor 3 (IRF3) and mediator of IRF3 activation (MITA) by TBK1. These findings suggest that zebrafish FGFR3 is a negative regulator of IFN by attenuating the kinase activity of TBK1, leading to the suppression of IFN expression.

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  • Authors+Show Affiliations

    ,

    Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China; University of Chinese Academy of Sciences, Beijing, China.

    ,

    Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China.

    ,

    Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China; University of Chinese Academy of Sciences, Beijing, China.

    ,

    Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China. Electronic address: bob@ihb.ac.cn.

    Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China; State Key Laboratory of Agricultural Microbiology, College of Fisheries, Huazhong Agricultural University, Wuhan, China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao, China. Electronic address: yzhang@ihb.ac.cn.

    Source

    Fish & shellfish immunology 92: 2019 Jun 11 pg 224-229

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    31200068

    Citation

    Liu, Shu-Bo, et al. "Zebrafish FGFR3 Is a Negative Regulator of RLR Pathway to Decrease IFN Expression." Fish & Shellfish Immunology, vol. 92, 2019, pp. 224-229.
    Liu SB, Lu LF, Lu XB, et al. Zebrafish FGFR3 is a negative regulator of RLR pathway to decrease IFN expression. Fish Shellfish Immunol. 2019;92:224-229.
    Liu, S. B., Lu, L. F., Lu, X. B., Li, S., & Zhang, Y. A. (2019). Zebrafish FGFR3 is a negative regulator of RLR pathway to decrease IFN expression. Fish & Shellfish Immunology, 92, pp. 224-229. doi:10.1016/j.fsi.2019.06.002.
    Liu SB, et al. Zebrafish FGFR3 Is a Negative Regulator of RLR Pathway to Decrease IFN Expression. Fish Shellfish Immunol. 2019 Jun 11;92:224-229. PubMed PMID: 31200068.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Zebrafish FGFR3 is a negative regulator of RLR pathway to decrease IFN expression. AU - Liu,Shu-Bo, AU - Lu,Long-Feng, AU - Lu,Xiao-Bing, AU - Li,Shun, AU - Zhang,Yong-An, Y1 - 2019/06/11/ PY - 2019/01/26/received PY - 2019/05/30/revised PY - 2019/06/04/accepted PY - 2019/6/15/pubmed PY - 2019/6/15/medline PY - 2019/6/15/entrez KW - FGFR3 KW - Interferon KW - Negative regulator KW - TBK1 KW - Zebrafish SP - 224 EP - 229 JF - Fish & shellfish immunology JO - Fish Shellfish Immunol. VL - 92 N2 - Fibroblast growth factor receptor (FGFR) 3 is one of the four distinct membrane-spanning tyrosine kinases required for proper skeletal development. In fish, the role of FGFR3 is still unclear. In this article, we reveal that zebrafish FGFR3 is a negative regulator of interferon (IFN) production in the innate immune response by suppressing the activity of TANK-binding kinase 1 (TBK1) in the process of virus infection. qPCR experiments demonstrate that the transcriptional level of cellular FGFR3 was upregulated by infection with spring viremia of carp virus (SVCV), indicating that FGFR3 might be involved in the process of host cell response to viral infection. Then, overexpression of FGFR3 significantly impeded the IFN promoter activity induced by a stimulator. In addition, the capabilities of a retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) system to activate IFN promoter were decreased during the overexpression of FGFR3. Subsequently, FGFR3 decreased the phosphorylation of interferon regulatory factor 3 (IRF3) and mediator of IRF3 activation (MITA) by TBK1. These findings suggest that zebrafish FGFR3 is a negative regulator of IFN by attenuating the kinase activity of TBK1, leading to the suppression of IFN expression. SN - 1095-9947 UR - https://www.unboundmedicine.com/medline/citation/31200068/Zebrafish_FGFR3_is_a_negative_regulator_of_RLR_pathway_to_decrease_IFN_expression L2 - https://linkinghub.elsevier.com/retrieve/pii/S1050-4648(19)30643-6 DB - PRIME DP - Unbound Medicine ER -