PUBLICATION
Zebrafish FGFR3 is a negative regulator of RLR pathway to decrease IFN expression
- Authors
- Liu, S.B., Lu, L.F., Lu, X.B., Li, S., Zhang, Y.A.
- ID
- ZDB-PUB-190615-14
- Date
- 2019
- Source
- Fish & shellfish immunology 92: 224-229 (Journal)
- Registered Authors
- Keywords
- FGFR3, Interferon, Negative regulator, TBK1, Zebrafish
- MeSH Terms
-
- Animals
- Fish Diseases/immunology*
- Immunity, Innate/genetics*
- Interferons/genetics*
- Interferons/metabolism
- Protein Serine-Threonine Kinases/genetics*
- Protein Serine-Threonine Kinases/immunology
- Receptor, Fibroblast Growth Factor, Type 3/genetics*
- Receptor, Fibroblast Growth Factor, Type 3/immunology
- Rhabdoviridae/physiology
- Rhabdoviridae Infections/immunology
- Rhabdoviridae Infections/veterinary
- Signal Transduction/immunology
- Zebrafish/genetics
- Zebrafish/immunology*
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/immunology
- Zebrafish Proteins/physiology
- PubMed
- 31200068 Full text @ Fish Shellfish Immunol.
Citation
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. 92:224-229.
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping