期刊
NATURE IMMUNOLOGY
卷 12, 期 2, 页码 137-U46出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1979
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资金
- Swiss National Science Foundation
- European Commission (TOLERAGE)
- Novartis Foundation for Biomedical Research, Switzerland
- German Ministry of Education and Research
- Austrian Science Fund [FWF J3044]
- Deutsche Forschungsgemeinschaft
- National Institutes of Health [AI060915, AI085089, U54 AI081680]
- Medical Research Council
- Wellcome Trust
- Biotechnology and Biological Sciences Research Council [BB/G012067/1] Funding Source: researchfish
- BBSRC [BB/G012067/1] Funding Source: UKRI
The 5' cap structures of higher eukaryote mRNAs have ribose 2'-O-methylation. Likewise, many viruses that replicate in the cytoplasm of eukaryotes have evolved 2'-O-methyltransferases to autonomously modify their mRNAs. However, a defined biological role for 2'-O-methylation of mRNA remains elusive. Here we show that 2'-O-methylation of viral mRNA was critically involved in subverting the induction of type I interferon. We demonstrate that human and mouse coronavirus mutants lacking 2'-O-methyltransferase activity induced higher expression of type I interferon and were highly sensitive to type I interferon. Notably, the induction of type I interferon by viruses deficient in 2'-O-methyltransferase was dependent on the cytoplasmic RNA sensor Mda5. This link between Mda5-mediated sensing of viral RNA and 2'-O-methylation of mRNA suggests that RNA modifications such as 2'-O-methylation provide a molecular signature for the discrimination of self and non-self mRNA.
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