PUBLICATION

Zebrafish sirt5 Negatively Regulates Antiviral Innate Immunity by Attenuating Phosphorylation and Ubiquitination of mavs

Authors
Chen, X., Fan, S., Zhu, C., Liao, Q., Tang, J., Yu, G., Cai, X., Ouyang, G., Xiao, W., Liu, X.
ID
ZDB-PUB-220825-5
Date
2022
Source
Journal of immunology (Baltimore, Md. : 1950)   209(6): 1165-1172 (Journal)
Registered Authors
Ouyang, Gang, Xiao, Wuhan, Yu, Guangqing
Keywords
none
MeSH Terms
  • Adaptor Proteins, Signal Transducing/genetics
  • Adaptor Proteins, Signal Transducing/metabolism
  • Animals
  • Antiviral Agents
  • Immunity, Innate
  • Phosphorylation
  • Rhabdoviridae
  • Sirtuins*/metabolism
  • Tretinoin/metabolism
  • Ubiquitination
  • Zebrafish*/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
36002231 Full text @ J. Immunol.
Abstract
The signaling adaptor MAVS is a critical determinant in retinoic acid-inducible gene 1-like receptor signaling, and its activation is tightly controlled by multiple mechanisms in response to viral infection, including phosphorylation and ubiquitination. In this article, we demonstrate that zebrafish sirt5, one of the sirtuin family proteins, negatively regulates mavs-mediated antiviral innate immunity. Sirt5 is induced by spring viremia of carp virus (SVCV) infection and binds to mavs, resulting in attenuating phosphorylation and ubiquitination of mavs. Disruption of sirt5 in zebrafish promotes survival ratio after challenge with SVCV. Consistently, the antiviral responsive genes are enhanced, and the replication of SVCV is diminished in sirt5-dificient zebrafish. Therefore, we reveal a function of zebrafish sirt5 in the negative regulation of antiviral innate immunity by targeting mavs.
Errata / Notes
https://www.jimmunol.org/content/209/6/1165
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping