PUBLICATION
Spring viraemia of carp virus modulates p53 expression using two distinct mechanisms
- Authors
- Li, S., Lu, L.F., Liu, S.B., Zhang, C., Li, Z.C., Zhou, X.Y., Zhang, Y.A.
- ID
- ZDB-PUB-190425-1
- Date
- 2019
- Source
- PLoS pathogens 15: e1007695 (Journal)
- Registered Authors
- Keywords
- none
- MeSH Terms
-
- Animals
- Cell Cycle Checkpoints/physiology
- DNA Viruses
- Fish Diseases
- Gene Expression Regulation, Viral/genetics
- HEK293 Cells
- Humans
- Immunity, Innate
- Rhabdoviridae/metabolism*
- Rhabdoviridae/pathogenicity
- Tumor Suppressor Protein p53/genetics*
- Tumor Suppressor Protein p53/metabolism*
- Ubiquitination
- Viremia
- Zebrafish
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 30925159 Full text @ PLoS Pathog.
Citation
Li, S., Lu, L.F., Liu, S.B., Zhang, C., Li, Z.C., Zhou, X.Y., Zhang, Y.A. (2019) Spring viraemia of carp virus modulates p53 expression using two distinct mechanisms. PLoS pathogens. 15:e1007695.
Abstract
p53, which regulates cell-cycle arrest and apoptosis, is a crucial target for viruses to release cells from cell-cycle checkpoints or to protect cells from apoptosis for their own benefit. Viral evasion mechanisms of aquatic viruses remain mysterious. Here, we report the spring viremia of carp virus (SVCV) degrading and stabilizing p53 in the ubiquitin-proteasome pathway by the N and P proteins, respectively. Early in an SVCV infection, significant induction was observed in the S phase and p53 was decreased in the protein level. Further experiments demonstrated that p53 interacted with SVCV N protein and was degraded by suppressing the K63-linked ubiquitination. However, the increase of p53 was observed late in the infection and experiments suggested that p53 was bound to SVCV P protein and stabilized by enhancing the K63-linked ubiquitination. Finally, lysine residue 358 was the key site for p53 K63-linked ubiquitination by the N and P proteins. Thus, our findings suggest that fish p53 is modulated by SVCV N and P protein in two distinct mechanisms, which uncovers the strategy for the subversion of p53-mediated host innate immune responses by aquatic viruses.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping