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Title: The RNA binding protein Quaking represses splicing of the Fibronectin EDA exon and downregulates the interferon response
Authors: Liao, Kuo-Chieh 
Chuo, Vanessa 
Fagg, W. Samuel
Modahl, Cassandra M. 
Widen, Steven
Garcia-Blanco, Mariano A. 
Issue Date: 24-Aug-2021
Publisher: Oxford University Press
Citation: Liao, Kuo-Chieh, Chuo, Vanessa, Fagg, W. Samuel, Modahl, Cassandra M., Widen, Steven, Garcia-Blanco, Mariano A. (2021-08-24). The RNA binding protein Quaking represses splicing of the Fibronectin EDA exon and downregulates the interferon response. Nucleic Acids Research 49 (17) : 10034-10045. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Quaking (QKI) controls RNA metabolism in many biological processes including innate immunity, where its roles remain incompletely understood. To illuminate these roles, we performed genome scale transcriptome profiling in QKI knockout cells with or without poly(I:C) transfection, a double-stranded RNA analog that mimics viral infection. Analysis of RNA-sequencing data shows that QKI knockout upregulates genes induced by interferons, suggesting that QKI is an immune suppressor. Furthermore, differential splicing analysis shows that QKI primarily controls cassette exons, and among these events, we noted that QKI silences splicing of the extra domain A (EDA) exon in fibronectin (FN1) transcripts. QKI knockout results in elevated production and secretion of FN1-EDA protein, which is a known activator of interferons. Consistent with an upregulation of the interferon response in QKI knockout cells, our results show reduced production of dengue virus-2 and Japanese encephalitis virus in these cells. In conclusion, we demonstrate that QKI downregulates the interferon system and attenuates the antiviral state. © 2021 The Author(s) 2021. Published by Oxford University Press on behalf of Nucleic Acids Research.
Source Title: Nucleic Acids Research
ISSN: 0305-1048
DOI: 10.1093/nar/gkab732
Rights: Attribution 4.0 International
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