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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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The RNA binding protein Quaking represses host interferon response by downregulating MAVS
Kuo-Chieh Liao1, Vanessa Chuo1, W Samuel Fagg2,3
1Programme in Emerging Infectious Diseases, Duke-NUS Medical School, Singapore.
RNA Biology
|December 13, 2019
Summary
Quaking (QKI) protein negatively regulates the host interferon response. QKI ablation enhances IFNβ transcription by upregulating MAVS, while QKI-5 isoform rescues this effect.
Area of Science:
- Immunology
- Molecular Biology
- Virology
Background:
- Quaking (QKI) is an RNA-binding protein (RBP) with known immune functions.
- Its precise role in regulating the host interferon (IFN) response is not well understood.
Purpose of the Study:
- To investigate the role of QKI in the host IFN response.
- To elucidate the molecular mechanisms by which QKI influences IFN signaling.
Main Methods:
- QKI knockout (KO) cell lines were generated.
- IFNβ transcription, IRF3 phosphorylation, and MAVS, RIG-I, and MDA5 levels were analyzed.
- Complementation studies with QKI isoforms and gene depletion/knockout experiments were performed.
Main Results:
- QKI ablation enhanced poly(I:C) and viral infection-induced IFNβ transcription.
- QKI KO cells showed increased IRF3 phosphorylation and MAVS upregulation.
- Complementation with QKI-5 isoform rescued the phenotype; MAVS depletion abolished IFNβ induction.
Conclusions:
- QKI negatively regulates the host IFN response.
- QKI represses IFN signaling by downregulating MAVS levels.
- This study reveals a novel mechanism of QKI in innate immunity.
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