PUBLICATION
Ubiquitin-specific protease 5 was involved in the interferon response to RGNNV in sea perch (Lateolabrax japonicus)
- Authors
- Jia, P., Zhang, W., Xiang, Y., Lu, X., Liu, W., Jia, K., Yi, M.
- ID
- ZDB-PUB-200522-8
- Date
- 2020
- Source
- Fish & shellfish immunology 103: 239-247 (Journal)
- Registered Authors
- Liu, Wei, Yi, Meisheng
- Keywords
- Lateolabrax japonicus, Nervous necrosis virus, RLRs signaling pathway, Ubiquitin-specific protease 5
- MeSH Terms
-
- Amino Acid Sequence
- Animals
- Base Sequence
- Fish Diseases/immunology*
- Fish Proteins/chemistry
- Fish Proteins/genetics
- Fish Proteins/immunology
- Gene Expression Profiling/veterinary
- Gene Expression Regulation/immunology*
- Immunity, Innate/genetics*
- Nodaviridae/physiology
- Perciformes/genetics*
- Perciformes/immunology*
- Phylogeny
- RNA Virus Infections/immunology
- RNA Virus Infections/veterinary
- Ubiquitin-Specific Proteases/chemistry
- Ubiquitin-Specific Proteases/genetics*
- Ubiquitin-Specific Proteases/immunology*
- PubMed
- 32437860 Full text @ Fish Shellfish Immunol.
Citation
Jia, P., Zhang, W., Xiang, Y., Lu, X., Liu, W., Jia, K., Yi, M. (2020) Ubiquitin-specific protease 5 was involved in the interferon response to RGNNV in sea perch (Lateolabrax japonicus). Fish & shellfish immunology. 103:239-247.
Abstract
Deubiquitinases are widely involved in the regulation of the virus-triggered type I interferon (IFN) signaling. Here, we found sea perch (Lateolabrax japonicus) ubiquitin-specific protease 5 (LjUSP5) was a negative regulatory factor of the red-spotted grouper nervous necrosis virus (RGNNV)-triggered IFN response. LjUSP5 encoded a polypeptide of 830 amino acids, containing a zinc finger UBP domain (residues 197-270 aa), two ubiquitin-associated domains (residues 593-607 aa; 628-665 aa), and one UBP domain (residues 782-807 aa), and shared the closest genetic relationship with the USP5 of Larimichthys crocea. Quantitative RT-PCR analysis showed that LjUSP5 was ubiquitously expressed and up-regulated significantly in all inspected tissues post RGNNV infection, and its transcripts significantly increased in brain, liver and kidney tissues post RGNNV infection. LjUSP5 was up-regulated in cultured LJB cells after poly I:C and RGNNV treatments. In addition, overexpression of LjUSP5 significantly inhibited the activation of zebrafish IFN 1 promoter and promoted RGNNV replication in vitro. Furthermore, LjUSP5 inhibited the activation of zebrafish IFN 1 promoter induced by key genes of retinoic acid-inducible gene I-like receptors signaling pathway. Our findings provides useful information for further elucidating the mechanism underlying NNV infection.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping