PUBLICATION
Tiger Frog Virus ORF080L Protein Interacts with LITAF and Impairs EGF-induced EGFR Degradation
- Authors
- Chen, Y.S., Chen, N.N., Qin, X.W., Mi, S., He, J., Lin, Y.F., Weng, S.P., Guo, C.J., Heb, J.G.
- ID
- ZDB-PUB-160310-8
- Date
- 2016
- Source
- Virus research 217: 133-42 (Journal)
- Registered Authors
- Keywords
- Endosome-lysosome pathway, Iridovirus, LITAF, Tiger frog virus, Viral replication
- MeSH Terms
-
- Animals
- Endosomes/metabolism
- Epidermal Growth Factor/metabolism
- HEK293 Cells
- HeLa Cells
- Hep G2 Cells
- Humans
- Lysosomes/metabolism
- Mice
- Proteolysis/drug effects
- Ranavirus/genetics
- Ranavirus/metabolism
- Ranavirus/pathogenicity*
- Real-Time Polymerase Chain Reaction
- Sequence Analysis, Protein
- Transcription, Genetic
- Tumor Necrosis Factor-alpha/metabolism*
- Viral Structural Proteins/metabolism
- Viral Structural Proteins/pharmacology*
- Virion
- Virus Replication
- PubMed
- 26956473 Full text @ Virus Res.
Citation
Chen, Y.S., Chen, N.N., Qin, X.W., Mi, S., He, J., Lin, Y.F., Weng, S.P., Guo, C.J., Heb, J.G. (2016) Tiger Frog Virus ORF080L Protein Interacts with LITAF and Impairs EGF-induced EGFR Degradation. Virus research. 217:133-42.
Abstract
Tiger frog virus (TFV) belongs to the genus Ranavirus, family Iridoviridae, and causes severe mortality in commercial cultures in China. TFV ORF080L is a gene homolog of lipopolysaccharide-induced TNF-α factor (LITAF), which is a regulator in endosome-to-lysosome trafficking through its function in the endosomal sorting complex required for transport machinery. The characteristics and biological roles of TFV ORF080L were identified. TFV ORF080L was predicted to encode an 84-amino acid peptide (VP080L). It had high-sequence identity with mammalian LITAF, but lacked the N-terminus of LITAF, which contains two PPXY motifs. Transcription and protein level analyses showed that TFV ORF080L was a late viral gene. Localization in the virons also showed that TFV VP080L was a viral structural protein. Immunofluorescence staining showed that TFV ORF080L was predominantly colocalized with plasma membrane and partly distributed with the late endosome in infected HepG2 cells. SiRNA-mediated TFV ORF080L silencing decreased viral reproduction. Moreover, TFV ORF080L interacted with human/zebrafish LITAF and impaired EGF-induced EGFR degradation, thereby indicating that TFV ORF080L played a role in endosome-to-lysosome trafficking. These findings suggested that TFV ORF080L might negate the function of cellular LITAF to impair endosomal sorting and trafficking. Results provide a clue to the link between the dysregulated endosomal trafficking and iridovirus pathogenesis.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping