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Next Generation Sequencing Facilitates Quantitative Analysis Of Wild Type And Tbk1 N129D KI Murine Embryonic Fibroblast Transcriptomes

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis Of Wild Type And Tbk1 N129D KI Murine Embryonic Fibroblast Transcriptomes

PROVIDER: PRJNA590207 | ENA |

REPOSITORIES: ENA

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Next Generation Sequencing Facilitates Quantitative Analysis Of Wild Type And Tbk1 N129D KI Murine Embryonic Fibroblast Transcriptomes

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TBK1-METTL3 axis facilitates antiviral immunity [MeRIP-seq]

Project description:TBK1-METTL3 axis facilitates antiviral immunity [MeRIP-seq]

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Gene regulation in ki-ras transfected murine fibroblasts

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Project description:mRNA m6A modification is involved in regulation of immune system. However, its function in antiviral immunity is controversial, and how immune responses regulate m6A modification is unknown. We here found TBK1, a key kinase of antiviral pathways, phosphorylated the core m6A methyltransferase METTL3 at Serine 67. The phosphorylated METTL3 interacted with translational complex and enhanced proteins translation, including IRF3, and facilitated antiviral responses. TBK1 also promoted METTL3 activation and m6A modification, which is required for stabilizing IRF3 mRNA. Type I IFN induction was severely impaired in METTL3 deficient cells. Mettl3flfl-lyz2-Cre mice were significantly more susceptible to IAV-induced lethality than control mice. Consistently, Ythdf1—/— mice cannot control viral infection and showed higher mortality than control mice due to decreased IRF3 expression. Together, we demonstrated that innate signals activated METTL3 via TBK1, and METTL3 and m6A modification secured antiviral immunity by promoting mRNA stability and protein translation.

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In vitro responses of fibroblasts from patients with TBK1 deficiency after TLR3 dependent and independent stimuli

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