Evidence map›Paper›PMID 30104661›Full record

ArticleNature structural & molecular biology2018

Terminal uridylyltransferases target RNA viruses as part of the innate immune system.

Jérémie Le Pen, Hongbing Jiang, Tomás Di Domenico, Emma Kneuss, Joanna Kosałka, Christian Leung, Marcos Morgan, Christian Much, Konrad L M Rudolph, Anton J Enright and 3 more

Open access · greenAbstract read
In one paragraph

Article in Nature structural & molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
4.5field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

74 citing papers in PubMed, 112 citations in OpenAlex.

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14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 4 countries.

Jérémie Le PenGurdon Institute, University of Cambridge, Cambridge, UK.
Hongbing JiangDepartments of Molecular Microbiology and Pathology & Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Tomás Di DomenicoGurdon Institute, University of Cambridge, Cambridge, UK.
Emma KneussGurdon Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0003-0662-8539
Joanna KosałkaGurdon Institute, University of Cambridge, Cambridge, UK.
Christian LeungDepartments of Molecular Microbiology and Pathology & Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Marcos MorganMRC Centre for Regenerative Medicine, Institute for Stem Cell Research, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.
Christian MuchMRC Centre for Regenerative Medicine, Institute for Stem Cell Research, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0002-1644-8200
Konrad L M RudolphGurdon Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-9866-7051
Anton J EnrightEMBL, European Bioinformatics Institute (EBI), Hinxton, UK.ORCID http://orcid.org/0000-0002-6090-3100
Dónal O'CarrollMRC Centre for Regenerative Medicine, Institute for Stem Cell Research, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0002-8626-2217
David WangDepartments of Molecular Microbiology and Pathology & Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Eric A MiskaGurdon Institute, University of Cambridge, Cambridge, UK. eam29@cam.ac.uk.ORCID http://orcid.org/0000-0002-4450-576X
University of Cambridge · GBMRC Centre for Regenerative Medicine · GBWashington University in St. Louis · USEuropean Bioinformatics Institute · GB

Funding

Cancer Research UK 11832Cancer Research UK 18583Cancer Research UK 21143Cancer Research UK A14492Cancer Research UK A18583European Research Council 260688Medical Research Council MR/K017047/1Wellcome Trust 092096Wellcome Trust 093970
6 · The paper itself

Abstract

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.

Indexed as

Immunity, InnateA549 CellsAnimalsCaenorhabditis elegansHumansRNA InterferenceRNA NucleotidyltransferasesRNA, ViralRNA VirusesTranscriptomeVirus ReplicationRNA NucleotidyltransferasesRNA, ViralUTP-RNA uridylyltransferase

Identifiers

PMID30104661
PMCPMC6130846
OpenAlexW2886199939

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.