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

Shu-Bo Liu1, Long-Feng Lu2, Xiao-Bing Lu1

  • 1Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China; University of Chinese Academy of Sciences, Beijing, China.

Fish & Shellfish Immunology
|June 15, 2019
PubMed
Summary
This summary is machine-generated.

Zebrafish Fibroblast Growth Factor Receptor (FGFR) 3 negatively regulates interferon production during viral infections. It suppresses TANK-binding kinase 1 (TBK1) activity, dampening the innate immune response.

Keywords:
FGFR3InterferonNegative regulatorTBK1Zebrafish

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Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Fibroblast Growth Factor Receptor (FGFR) 3 is crucial for skeletal development.
  • The function of FGFR3 in fish immunity, particularly in response to viral infections, remains largely unknown.

Purpose of the Study:

  • To investigate the role of zebrafish FGFR3 in the innate immune response against viral infections.
  • To elucidate the molecular mechanism by which FGFR3 influences interferon production.

Main Methods:

  • Quantitative PCR (qPCR) to assess FGFR3 gene expression.
  • Overexpression studies to evaluate the impact of FGFR3 on interferon promoter activity.
  • Western blotting to analyze the phosphorylation of key signaling proteins (IRF3, MITA).

Main Results:

  • Zebrafish FGFR3 expression is upregulated upon infection with Spring Viremia of Carp Virus (SVCV).
  • Overexpression of FGFR3 significantly inhibits virus-induced interferon promoter activity and the RIG-I-like receptor (RLR) signaling pathway.
  • FGFR3 suppresses the activation of TANK-binding kinase 1 (TBK1), leading to decreased phosphorylation of IRF3 and MITA.

Conclusions:

  • Zebrafish FGFR3 acts as a negative regulator of interferon production in the innate immune response.
  • FGFR3 attenuates TBK1 kinase activity, thereby suppressing interferon expression during viral infections.