PUBLICATION

Comparative transcriptome analysis reveals the role of p53 signalling pathway during red-spotted grouper nervous necrosis virus infection in Lateolabrax japonicus brain cells

Authors
Xiang, Y., Jia, P., Liu, W., Yi, M., Jia, K.
ID
ZDB-PUB-190120-4
Date
2019
Source
Journal of fish diseases   42(4): 585-595 (Journal)
Registered Authors
Liu, Wei, Yi, Meisheng
Keywords
Lateolabrax japonicas, apoptosis, p53, red-spotted grouper nervous necrosis virus, transcriptome
MeSH Terms
  • Animals
  • Apoptosis/genetics
  • Brain/cytology
  • Brain/virology*
  • Down-Regulation
  • Gene Expression Profiling*
  • High-Throughput Nucleotide Sequencing
  • Nodaviridae
  • Perches/virology*
  • RNA Virus Infections/immunology
  • RNA Virus Infections/veterinary*
  • RNA Virus Infections/virology
  • Signal Transduction
  • Tumor Suppressor Protein p53/genetics*
  • Tumor Suppressor Protein p53/metabolism
  • Up-Regulation
PubMed
30659619 Full text @ J. Fish Dis.
Abstract
Nervous necrosis virus (NNV) is one of the fish pathogens that have caused mass mortalities of many marine and freshwater fishes in the world. To better comprehend the molecular immune mechanism of sea perch (Lateolabrax japonicus) against NNV infection, the comparative transcriptome analysis of red-spotted grouper nervous necrosis virus (RGNNV)-infected or mock-infected L. japonicus brain (LJB) cells was performed via RNA sequencing technology. Here, 1,969 up-regulated genes and 9,858 down-regulated genes, which were widely implicated in immune response pathways, were identified. Furthermore, we confirmed that p53 signalling pathway was repressed at 48 hr post-RGNNV infection, as indicated by up-regulation of Mdm2 and down-regulation of p53 and its downstream target genes, including Bax, Casp8 and CytC. Overexpression of L. japonicus p53 (Ljp53) significantly inhibited RGNNV replication and up-regulated the expression of apoptosis-related genes, whereas the down-regulation caused by pifithrin-α led to the opposite effect, suggesting Ljp53 might promote cell apoptosis to repress virus replication. Luciferase assay indicated that Ljp53 could enhance the promoter activities of zebrafish interferon (IFN)1, indicating that Ljp53 could exert its anti-RGNNV activities by enforcing the type I IFN response. This study revealed the potential antiviral role of p53 during NNV infection.
Genes / Markers
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping