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Smarcad1 coordinates innate immunity-linked gene expression in the intestinal epithelium

ABSTRACT: Smarcad1 coordinates innate immunity-linked gene expression in the intestinal epithelium

PROVIDER: PRJNA524917 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8646240.fastq.gz	Fastqsanger.gz
	SRR8646250.fastq.gz	Fastqsanger.gz
	SRR8646260.fastq.gz	Fastqsanger.gz
	SRR8646270_1.fastq.gz	Fastqsanger.gz
	SRR8646270_2.fastq.gz	Fastqsanger.gz

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Smarcad1 coordinates innate immunity-linked gene expression in the intestinal epithelium [wCO RNA-seq]

Project description:Smarcad1 is one of the most conserved chromatin remodelling factors, from yeast to human, with suggested functions in gene silencing, heterochromatin maintenance and genome stability. However, its role in tissue function is poorly understood. As this factor is highly expressed in the stem- and proliferative zone in the intestinal epithelium, we explored the role of this factor in this tissue. Specific deletion of Smarcad1 in the intestinal epithelium led to colitis resistance in the dextran sodium sulphate colitis model. Intestine tissue-specific deletion of Smarcad1 resulted in notable changes in gene expression in the small intestine, colon and organoids from small intestine. Strikingly, we found an increase of expression of several genes linked to innate immunity. Our study demonstrates that an innate immunity response can be coordinated by a chromatin remodelling factor. It highlights the role of intestinal epithelial cells in the colitis response and we identified candidate members of the gut microbiome that elicit an epithelial Smarcad1-dependent colitis response.

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Smarcad1 coordinates innate immunity-linked gene expression in the intestinal epithelium [ChIP-seq]

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Smarcad1 coordinates innate immunity-linked gene expression in the intestinal epithelium[SI RNA-seq]

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Smarcad1 coordinates innate immunity-linked gene expression in the intestinal epithelium [Cocr RNA-seq]

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Smarcad1 coordinates innate immunity-linked gene expression in the intestinal epithelium[SI RNA-seq]

Project description:Smarcad1 is one of the most conserved chromatin remodelling factors, from yeast to human, with suggested functions in gene silencing, heterochromatin maintenance and genome stability. However, its role in tissue function is poorly understood. As this factor is highly expressed in the stem- and proliferative zone in the intestinal epithelium, we explored the role of this factor in this tissue. Intestine tissue-specific deletion of Smarcad1 resulted in notable changes in gene expression in the small intestine, colon and organoids from small intestine. Strikingly, we found an increase of expression of several genes linked to innate immunity and a dramatic increase of a Bglap3 coding for an osteocalcin isoform, a protein normally expressed in osteoblasts. Our study demonstrates that an innate immunity response can be coordinated by a chromatin remodelling factor

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Smarcad1 coordinates innate immunity-linked gene expression in the intestinal epithelium [ChIP-seq]

Project description:How intestinal epithelial cells interact with the host immune system and the microbiota and how this is regulated at the gene expression level are critical questions. Smarcad1 is one of the most conserved chromatin remodelling factors, from yeast to human, with suggested functions in gene silencing, heterochromatin maintenance and genome stability. However, its role in tissue function is poorly understood. As this factor is highly expressed in the stem- and proliferative zone in the intestinal epithelium, we explored the role of this factor in this tissue. Specific deletion of Smarcad1 in the intestinal epithelium led to colitis resistance in the dextran sodium sulphate colitis model. Intestine tissue-specific deletion of Smarcad1 resulted in notable changes in gene expression in the small intestine and colon. Absence of Smarcad1 led to changes in chromatin accessibility and significant changes in histone H3K9me3 but not H3K9me2 over many sites, including many genes that are differentially regulated upon Smarcad1 deletion. Our study demonstrates that an innate immunity response can be coordinated by a chromatin remodelling factor.

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