Author: Xiang, Yangxi; Jia, Peng; Liu, Wei; Yi, Meisheng; Jia, Kuntong
Title: Comparative transcriptome analysis reveals the role of p53 signalling pathway during redâ€spotted grouper nervous necrosis virus infection in Lateolabrax japonicus brain cells Cord-id: 4buooi2d Document date: 2019_1_18
ID: 4buooi2d
Snippet: 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 redâ€spotted grouper nervous necrosis virus (RGNNV)â€infected or mockâ€infected L. japonicus brain (LJB) cells was performed via RNA sequencing technology. Here, 1,969 upâ€regulated genes and 9,858 d
Document: 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 redâ€spotted grouper nervous necrosis virus (RGNNV)â€infected or mockâ€infected L. japonicus brain (LJB) cells was performed via RNA sequencing technology. Here, 1,969 upâ€regulated genes and 9,858 downâ€regulated genes, which were widely implicated in immune response pathways, were identified. Furthermore, we confirmed that p53 signalling pathway was repressed at 48 hr postâ€RGNNV infection, as indicated by upâ€regulation of Mdm2 and downâ€regulation of p53 and its downstream target genes, including Bax, Casp8 and CytC. Overexpression of L. japonicus p53 (Ljp53) significantly inhibited RGNNV replication and upâ€regulated the expression of apoptosisâ€related genes, whereas the downâ€regulation caused by pifithrinâ€Î± 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 antiâ€RGNNV activities by enforcing the type I IFN response. This study revealed the potential antiviral role of p53 during NNV infection.
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