PUBLICATION

PLAAT1 inhibits type I interferon response via degradation of IRF3 and IRF7 in Zebrafish

Authors
Zhao, X., Huang, W., Shi, Y., Guo, J., Xiao, H., Ji, N., Feng, J., Dang, H., Zou, J.
ID
ZDB-PUB-220930-5
Date
2022
Source
Frontiers in immunology   13: 979919 (Journal)
Registered Authors
Keywords
IRF3, IRF7, PLAAT1, autophagy, interferon, virus
MeSH Terms
  • Animals
  • Antiviral Agents
  • Interferon Regulatory Factors/metabolism
  • Interferon Type I*/metabolism
  • Transglutaminases/metabolism
  • Tumor Suppressor Protein p53
  • Zebrafish/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
36172355 Full text @ Front Immunol
Abstract
PLAAT1 is a member of the PLAAT protein family and plays important roles in tumor suppression, transglutaminase activation and peroxisomal biogenesis. Recently, PLAAT1 has been shown to promote degradation of p53 protein and cellular organelles such as mitochondria, endoplasmic reticulum and lysosome. In this study, we show that PLAAT1 inhibits the production of type I interferon and promotes virus replication in zebrafish. Overexpression of Plaat1 in zebrafish cells suppresses antiviral responses and promotes virus replication. Mechanistically, PLAAT1 interacts with IRF3 and IRF7 to initiate degradation of IRF3 and IRF7, which can be attenuated by 3-methyladenine, an inhibitor of autophagosome. Our study provides novel insights into the functions of PLAAT1 in host immune response to viral infection.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping