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Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice [RNA-seq]

ABSTRACT: Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice [RNA-seq]

PROVIDER: PRJNA945900 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23891452.fastq.gz	Fastqsanger.gz
	SRR23891452_1.fastq.gz	Fastqsanger.gz
	SRR23891452_2.fastq.gz	Fastqsanger.gz
	SRR23891453.fastq.gz	Fastqsanger.gz
	SRR23891453_1.fastq.gz	Fastqsanger.gz

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Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice [ATAC-seq]

Project description:Microglia are the tissue resident macrophages of the central nervous system (CNS). Dysregulation of inflammatory processes in the CNS is associated with aging, and neurodegenerative diseases, where microglia acquire a sensitized, or primed, phenotype, which is characterized by an increased inflammatory phenotype and an exaggerated reactivity to immune challenges. Transcriptomic profiling of microglia in different neurodegenerative disease and aging mouse models identified a common, primed, gene expression signature. However, the transcriptional mechanisms that mediate microglia priming still remains unclear. In DNA repair deficient (Ercc1Δ/ko) mice, microglia acquire a profound primed phenotype and by integrating RNA-seq and ATAC-seq data of Ercc1Δ/ko microglia, we identified transcription factors IRF7, IRF9 and SMAD3 as possible core regulators of microglia priming. Our data suggest that increased IRF7/IRF9 activity and decreased SMAD3 activity might be important for microglia to acquire a primed gene signature. This study provides insight in the transcriptomic regulation of primed microglia, which are implicated in aging and neurodegenerative diseases.

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Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice [RNA-seq]

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Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice [ATAC-seq]

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Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice

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Effect of deletion of Irf3, Irf7 or Irf9 on gene expression in sgScd2 Th1 cells.

Project description:To investigate the role of the IRF family in the regulation of interferon stimulated genes, we conducted CRISPR/Cas9 mediated genome editing of Irf3, Irf7 or Irf9 in sgScd2 Th1 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of control, sgScd2, sgScd2/sgIrf3, sgScd2/sgIrf7 or sgScd2/sgIrf9 Th1 cells.

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