Journal
NATURE STRUCTURAL & MOLECULAR BIOLOGY
Volume 25, Issue 9, Pages 778-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41594-018-0106-9
Keywords
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Funding
- Cancer Research UK [C13474/A18583, C6946/A14492]
- Wellcome Trust [104640/Z/14/Z, 092096/Z/10/Z, 093970/Z/10/Z, 102452/Z/13/Z]
- The European Research Council (ERC) [260688]
- Pathogenesis of Infectious Disease Award from the Burroughs Wellcome Fund
- MRC [MR/K017047/1] Funding Source: UKRI
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RNA viruses are a major threat to animals and plants. RNA interference (RNAi) and the interferon response provide innate antiviral defense against RNA viruses. Here, we performed a large-scale screen using Caenorhabditis elegans and its natural pathogen the Orsay virus (OrV), and we identified cde-1 as important for antiviral defense. CDE-1 is a homolog of the mammalian TUT4 and TUT7 terminal uridylyltransferases (collectively called TUT4(7)); its catalytic activity is required for its antiviral function. CDE-1 uridylates the 3' end of the OrV RNA genome and promotes its degradation in a manner independent of the RNAi pathway. Likewise, TUT4(7) enzymes uridylate influenza A virus (IAV) mRNAs in mammalian cells. Deletion of TUT4(7) leads to increased IAV mRNA and protein levels. Collectively, these data implicate 3'-terminal uridylation of viral RNAs as a conserved antiviral defense mechanism.
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