USP18 positively regulates innate antiviral immunity by promoting K63-linked polyubiquitination of MAVS

Jinxiu Hou, Lulu Han, Ze Zhao, Huiqing Liu, Lei Zhang, Chunhong Ma, Fan Yi, Bingyu Liu, Yi Zheng () and Chengjiang Gao ()
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Jinxiu Hou: Shandong University
Lulu Han: Shandong University
Ze Zhao: Shandong University
Huiqing Liu: Shandong University
Lei Zhang: Shandong University
Chunhong Ma: Shandong University
Fan Yi: Shandong University
Bingyu Liu: Shandong University
Yi Zheng: Shandong University
Chengjiang Gao: Shandong University

Nature Communications, 2021, vol. 12, issue 1, 1-16

Abstract: Abstract Activation of MAVS, an adaptor molecule in Rig-I-like receptor (RLR) signaling, is indispensable for antiviral immunity, yet the molecular mechanisms modulating MAVS activation are not completely understood. Ubiquitination has a central function in regulating the activity of MAVS. Here, we demonstrate that a mitochondria-localized deubiquitinase USP18 specifically interacts with MAVS, promotes K63-linked polyubiquitination and subsequent aggregation of MAVS. USP18 upregulates the expression and production of type I interferon following infection with Sendai virus (SeV) or Encephalomyocarditis virus (EMCV). Mice with a deficiency of USP18 are more susceptible to RNA virus infection. USP18 functions as a scaffold protein to facilitate the re-localization of TRIM31 and enhances the interaction between TRIM31 and MAVS in mitochondria. Our results indicate that USP18 functions as a post-translational modulator of MAVS-mediated antiviral signaling.

Date: 2021
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DOI: 10.1038/s41467-021-23219-4

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