期刊
CELL REPORTS
卷 11, 期 8, 页码 1193-1207出版社
CELL PRESS
DOI: 10.1016/j.celrep.2015.04.047
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资金
- Kato Memorial Bioscience Foundation
- Ministry of Education, Science, and Culture
- Ministry of Health, Labor, and Welfare of Japan
- GI-CoRE project
- Grants-in-Aid for Scientific Research [15K08517] Funding Source: KAKEN
RIG-I-mediated type I interferon (IFN) production and nuclease-mediated viral RNA degradation are essential for antiviral innate immune responses. DDX60 is an IFN-inducible cytoplasmic helicase. Here, we report that DDX60 is a sentinel for both RIG-I activation and viral RNA degradation. We show that DDX60 is an upstream factor of RIG-I that activates RIG-I signaling in a ligand-specific manner. DDX60 knockout attenuates RIG-I signaling and significantly reduces virus-induced type I IFN production in vivo. In addition, we show that DDX60 is involved in RIG-I-independent viral RNA degradation. DDX60 and RIG-I adaptor MAVS double-knockout mice reveal a role for DDX60-dependent RNA degradation in antiviral responses. Several viruses induced DDX60 phosphorylation via epidermal growth factor receptor (EGFR), leading to attenuation of the DDX60 antiviral activities. Our results define DDX60 as a sentinel for cytoplasmic antiviral response, which is counteracted by virus-mediated EGF receptor activation.
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