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Epigenetic signals that direct cell type specific interferon beta response in mouse cells

ABSTRACT: Epigenetic signals that direct cell type specific interferon beta response in mouse cells

PROVIDER: PRJNA674372 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12974400.fastq.gz	Fastqsanger.gz
	SRR12974500.fastq.gz	Fastqsanger.gz
	SRR12974401.fastq.gz	Fastqsanger.gz
	SRR12974501.fastq.gz	Fastqsanger.gz
	SRR12974402.fastq.gz	Fastqsanger.gz

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Epigenetic signals that direct cell type specific interferon beta response in mouse cells

Project description:The antiviral response induced by type I interferon (IFN) via the JAK-STAT signaling cascade results in the activation of a set of IFN-stimulated genes (ISGs). This response varies between different cell types of the organism. However, the linkage between the underlying epigenetic features and innate immune response is not well understood. We mapped ISGs and STAT1 and STAT2 binding sites in mouse embryonic stem cells and differentiated cells before and after treatment with IFNβ together with histone acetylation (ac) and mono- and tri-methylation (me1, me3) marks at histone H3 lysine residues for H3K4me1, H3K4me3, H3K9ac, H3K27ac, H3K9me3 and H3K27me3. Many ISGs were cell type specific and displayed distinct STAT1/2 binding patterns at promoters. Furthermore, binding to putative enhancers at intergenic and intronic site was driving ISGs as inferred from a co-regulation analysis of open chromatin sites in single cells. Activator binding was dependent on the chromatin context and positively correlated with pre-existing H3K4me1 enrichment and open chromatin states while the presence of H3K27me3 had the opposite effect. Chromatin features present before stimulation direct the cell type specific response to type I IFNs. Thus, epigenetic signals represent an additional regulatory layer that is responsible for the tissue dependent activity of this signaling pathway. The mechanistic insight gained in our study could be exploited for modulating innate immune response during virus infection or cancer immunotherapy.

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Epigenetic signals that direct cell type-specific interferon beta response in mouse cells.

Project description:The antiviral response induced by type I interferon (IFN) via the JAK-STAT signaling cascade activates hundreds of IFN-stimulated genes (ISGs) across human and mouse tissues but varies between cell types. However, the links between the underlying epigenetic features and the ISG profile are not well understood. We mapped ISGs, binding sites of the STAT1 and STAT2 transcription factors, chromatin accessibility, and histone H3 lysine modification by acetylation (ac) and mono-/tri-methylation (me1, me3) in mouse embryonic stem cells and fibroblasts before and after IFNβ treatment. A large fraction of ISGs and STAT-binding sites was cell type specific with promoter binding of a STAT1/2 complex being a key driver of ISGs. Furthermore, STAT1/2 binding to putative enhancers induced ISGs as inferred from a chromatin co-accessibility analysis. STAT1/2 binding was dependent on the chromatin context and positively correlated with preexisting H3K4me1 and H3K27ac marks in an open chromatin state, whereas the presence of H3K27me3 had an inhibitory effect. Thus, chromatin features present before stimulation represent an additional regulatory layer for the cell type-specific antiviral response.

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