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USP18 recruits USP20 to promote innate antiviral response through deubiquitinating STING/MITA
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USP18 recruits USP20 to promote innate antiviral response through deubiquitinating STING/MITA
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Journal Article
USP18 recruits USP20 to promote innate antiviral response through deubiquitinating STING/MITA
2016
Overview
STING （also known as MITA） mediates the innate antiviral signaling and ubiquitination of STING is key to its function. However, the deubiquitination process of STING is unclear. Here we report that USP18 recruits USP20 to deconjugate K48-1inked ubiquitination chains from STING and promotes the stability of STING and the expression of type I IFNs and proinflammatory cytokines after DNA virus infection. USP18 deficiency or knockdown of USP20 resulted in enhanced K48-1inked ubiquitination and accelerated degradation of STING, and impaired activation of IRF3 and NF-κB as well as induction of downstream genes after infection with DNA virus HSV-1 or transfeetion of various DNA ligands. In addition, Uspl8-/- mice were more susceptible to HSV-1 infection compared with the wildtype littermates. USP18 did not deubiquitinate STING in vitro but facilitated USP20 to catalyze deubiquitination of STING in a manner independent of the enzymatic activity of USP18. In addition, reconstitution of STING into Uspl8-/- MEFs restored HSV-1-induced expression of downstream genes and cellular antiviral responses. Our findings thus uncover previously uncharacterized roles of USPI8 and USP20 in mediating virus-triggered signaling and contribute to the understanding of the complicated regulatory system of the innate antiviral responses.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Animals
/ Biomedical and Life Sciences
/ Bone Marrow Cells - cytology
/ Bone Marrow Cells - metabolism
/ Cytokines - antagonists & inhibitors
/ DNA
/ Genes
/ Herpesvirus 1, Human - physiology
/ Humans
/ Interferon regulatory factor 3
/ Interferon Regulatory Factor-3 - metabolism
/ Interferon Type I - metabolism
/ Membrane Proteins - metabolism
/ Mice
/ Original
/ Receptor, Interferon alpha-beta - deficiency
/ Receptor, Interferon alpha-beta - genetics
/ Ubiquitin Thiolesterase - antagonists & inhibitors
/ Ubiquitin Thiolesterase - genetics
/ Ubiquitin Thiolesterase - metabolism
/ Ubiquitins - antagonists & inhibitors
/ Viruses
