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TBK1-METTL3 axis facilitates antiviral immunity

ABSTRACT: TBK1-METTL3 axis facilitates antiviral immunity

PROVIDER: PRJNA669704 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12816830_1.fastq.gz	Fastqsanger.gz
	SRR12816830_2.fastq.gz	Fastqsanger.gz
	SRR12816831_1.fastq.gz	Fastqsanger.gz
	SRR12816831_2.fastq.gz	Fastqsanger.gz
	SRR12816832_1.fastq.gz	Fastqsanger.gz

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

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.

2020-11-04 | GSE160790 | GEO

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

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

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TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Brain from WT and Mettl3 heterozygous kd]

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.

2020-10-14 | GSE159421 | GEO

TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Mock or VSV treated WT and Mettl3 crispr iBMDM]

2020-10-19 | GSE159567 | GEO

TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Mock or VSV treated WT and Ythdf1-KO BMDM]

2020-10-31 | GSE160481 | GEO

TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Brain from WT and Mettl3 heterozygous kd]

Project description:TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Brain from WT and Mettl3 heterozygous kd]

| PRJNA668900 | ENA

TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Mock or VSV treated WT and Mettl3 crispr iBMDM]

Project description:TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Mock or VSV treated WT and Mettl3 crispr iBMDM]

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TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Mock or VSV treated WT and Ythdf1-KO BMDM]

Project description:TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Mock or VSV treated WT and Ythdf1-KO BMDM]

| PRJNA673356 | ENA

TBK1-METTL3 axis facilitates antiviral immunity

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-10-19 | GSE159568 | GEO

GSNOR facilitates antiviral innate immunity by restricting TBK1 cysteine S-nitrosation.

Project description:Innate immunity is the first line of host defense against pathogens. This process is modulated by multiple antiviral protein modifications, such as phosphorylation and ubiquitination. Here, we showed that cellular S-nitrosoglutathione reductase (GSNOR) is actively involved in innate immunity activation. GSNOR deficiency in mouse embryo fibroblasts (MEFs) and RAW264.7 macrophages reduced the antiviral innate immune response and facilitated herpes simplex virus-1 (HSV-1) and vesicular stomatitis virus (VSV) replication. Concordantly, HSV-1 infection in Gsnor-/- mice and wild-type mice with GSNOR being inhibited by N6022 resulted in higher mortality relative to the respective controls, together with severe infiltration of immune cells in the lungs. Mechanistically, GSNOR deficiency enhanced cellular TANK-binding kinase 1 (TBK1) protein S-nitrosation at the Cys423 site and inhibited TBK1 kinase activity, resulting in reduced interferon production for antiviral responses. Our study indicated that GSNOR is a critical regulator of antiviral responses and S-nitrosation is actively involved in innate immunity.

| S-EPMC8577438 | biostudies-literature

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