PUBLICATION

Zebrafish prmt2 Attenuates Antiviral Innate Immunity by Targeting traf6

Authors
Zhu, J., Li, X., Sun, X., Zhou, Z., Cai, X., Liu, X., Wang, J., Xiao, W.
ID
ZDB-PUB-211022-2
Date
2021
Source
Journal of immunology (Baltimore, Md. : 1950)   207(10): 2570-2580 (Journal)
Registered Authors
Wang, Jing, Xiao, Wuhan
Keywords
none
MeSH Terms
  • Animals
  • Immunity, Innate/immunology*
  • Protein-Arginine N-Methyltransferases/immunology*
  • Rhabdoviridae/immunology
  • Rhabdoviridae Infections/immunology*
  • TNF Receptor-Associated Factor 6/immunology*
  • Zebrafish
PubMed
34654690 Full text @ J. Immunol.
Abstract
TNFR-associated factor 6 (TRAF6) not only recruits TBK1/IKKε to MAVS upon virus infection but also catalyzes K63-linked polyubiquitination on substrate or itself, which is critical for NEMO-dependent and -independent TBK1/IKKε activation, leading to the production of type I IFNs. The regulation at the TRAF6 level could affect the activation of antiviral innate immunity. In this study, we demonstrate that zebrafish prmt2, a type I arginine methyltransferase, attenuates traf6-mediated antiviral response. Prmt2 binds to the C terminus of traf6 to catalyze arginine asymmetric dimethylation of traf6 at arginine 100, preventing its K63-linked autoubiquitination, which results in the suppression of traf6 activation. In addition, it seems that the N terminus of prmt2 competes with mavs for traf6 binding and prevents the recruitment of tbk1/ikkε to mavs. By zebrafish model, we show that loss of prmt2 promotes the survival ratio of zebrafish larvae after challenge with spring viremia of carp virus. Therefore, we reveal, to our knowledge, a novel function of prmt2 in the negative regulation of antiviral innate immunity by targeting traf6.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping