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The intestinal microbiota programs DNA methylation to control tissue homeostasis and inflammation [BiSulfite-seq]

ABSTRACT: The intestinal microbiota programs DNA methylation to control tissue homeostasis and inflammation [BiSulfite-seq]

PROVIDER: PRJNA518144 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8514890_1.fastq.gz	Fastqsanger.gz
	SRR8514890_2.fastq.gz	Fastqsanger.gz
	SRR8514891_1.fastq.gz	Fastqsanger.gz
	SRR8514891_2.fastq.gz	Fastqsanger.gz
	SRR8514892_1.fastq.gz	Fastqsanger.gz

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The intestinal microbiota programs DNA methylation to control tissue homeostasis and inflammation [BiSulfite-seq]

Project description:Although much research has been done on the diversity of gut microbiome, little is known about the way it influences intestinal homeostasis under normal and pathogenic conditions. Epigenetic mechanisms have recently been suggested as operating at the interface between the microbiota and the intestinal epithelium cells (IECs). Using genome-wide analyses, we discovered that exposure to microbiota induced both global DNA hypomethylation and localized changes at regulatory elements, which culminates in activation of a set of “early sentinel” response genes that play a role in maintaining gut homeostasis. Furthermore, we demonstrated that exposure to microbiota in acute inflammation results in profound DNA methylation and chromatin accessibility changes at regulatory elements leading to alterations in the gene expression program in colitis and colon cancer. Our studies add a new dimension to our understanding of the cross talk between the microbiota and IECs, and provide the foundation for how microbiota impact epigenetic programming.

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Project description:This study uses whole-genome bisulfite sequencing to characterize the methylomes of the AOM/DSS mouse model at single-base resolution. In this model, mice are treated with dextran sodium sulfate (DSS) to induce colitis. When this treatment is preceded by injections of the weak carcinogen azoxymethane (AOM) the mice develop intestinal tumors. Our results identify hypermethylated DMVs as a prominent feature of the colitis methylome that is conserved in intestinal adenocarcinomas. Further analyses reveal a subset of DMV-associated genes, expressed in normal intestinal epithelial cells, that were silenced and hypermethylated in inflamed and cancerous intestinal cells. Together, these findings provide strong support for the hypothesis that inflammatory signals induce a higher risk for cancer development by manipulating the epigenome. . Whole genome methylation analysis of M. musculus. Three conditions were sequenced analyzed, the first is an untreated control, the second corresponds to inflammation, the third to cancer induced by inflammation. All three conditions were analyzed using three replicates.

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The intestinal microbiota programs DNA methylation to control tissue homeostasis and inflammation

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

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