RNF115 plays dual roles in innate antiviral responses by catalyzing distinct ubiquitination of MAVS and MITA

Zhi-Dong Zhang, Tian-Chen Xiong, Shu-Qi Yao, Ming-Cong Wei, Ming Chen, Dandan Lin and Bo Zhong ()
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Zhi-Dong Zhang: Zhongnan Hospital of Wuhan University
Tian-Chen Xiong: Zhongnan Hospital of Wuhan University
Shu-Qi Yao: Zhongnan Hospital of Wuhan University
Ming-Cong Wei: Zhongnan Hospital of Wuhan University
Ming Chen: Zhongnan Hospital of Wuhan University
Dandan Lin: Renmin Hospital of Wuhan University
Bo Zhong: Zhongnan Hospital of Wuhan University

Nature Communications, 2020, vol. 11, issue 1, 1-17

Abstract: Abstract MAVS and MITA are essential adaptor proteins mediating innate antiviral immune responses against RNA and DNA viruses, respectively. Here we show that RNF115 plays dual roles in response to RNA or DNA virus infections by catalyzing distinct types of ubiquitination of MAVS and MITA at different phases of viral infection. RNF115 constitutively interacts with and induces K48-linked ubiquitination and proteasomal degradation of homeostatic MAVS in uninfected cells, whereas associates with and catalyzes K63-linked ubiquitination of MITA after HSV-1 infection. Consistently, the protein levels of MAVS are substantially increased in Rnf115−/− organs or cells without viral infection, and HSV-1-induced aggregation of MITA is impaired in Rnf115−/− cells compared to the wild-type counterparts. Consequently, the Rnf115−/− mice exhibit hypo- and hyper-sensitivity to EMCV and HSV-1 infection, respectively. These findings highlight dual regulation of cellular antiviral responses by RNF115-mediated ubiquitination of MAVS and MITA and contribute to our understanding of innate immune signaling.

Date: 2020
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DOI: 10.1038/s41467-020-19318-3

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