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DNA methylation, through DNMT1, has an essential role in the development of gastrointestinal smooth muscle cells and disease (BiSulfite-seq)

ABSTRACT: DNA methylation, through DNMT1, has an essential role in the development of gastrointestinal smooth muscle cells and disease (BiSulfite-seq)

PROVIDER: PRJNA431590 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6511543_1.fastq.gz	Fastqsanger.gz
	SRR6511543_2.fastq.gz	Fastqsanger.gz
	SRR6511544_1.fastq.gz	Fastqsanger.gz
	SRR6511544_2.fastq.gz	Fastqsanger.gz

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DNA methylation, through DNMT1, has an essential role in the development of gastrointestinal smooth muscle cells and disease (BiSulfite-seq)

Project description:DNA methylation is a key epigenetic modification that can regulate gene expression. Genomic DNA hypomethylation is commonly found in many gastrointestinal (GI) diseases. Dysregulated gene expression in GI smooth muscle cells (GI-SMC) can lead to motility disorders. However, the consequences of genomic DNA hypomethylation within GI-SMC are still elusive. Utilizing a Cre-lox murine model, we have generated SMC-restricted DNA methyltransferase 1 (Dnmt1) knockout (KO) mice and analyzed the effects of Dnmt1 deficiency. Dnmt1-KO pups are born smaller than their wild type littermates, have shortened GI tracts, lose peristaltic movement due to loss of the tunica muscularis in their intestine, causing massive intestinal dilation, and death around post-natal day 21. Within smooth muscle tissue, significant CpG hypomethylation occurs across the genome at promoters, introns and exons. Additionally, there is a marked loss of differentiated SMC markers (Srf, Myh11, miR-133, miR-143/145), an increase in pro-apoptotic markers (Nr4a1, Gadd45g), loss of cellular connectivity, and an accumulation of coated vesicles within SMC. Interestingly, we observed consistent abnormal expression patterns of enzymes involved in DNA methylation between both ¬Dnmt1-KO mice and diseased human GI tissue. These data demonstrate that DNA hypomethylation in embryonic SMC, via congenital Dnmt1 deficiency, contributes to massive dysregulation of gene expression and is lethal to GI-SMC. These results suggest that Dnmt1 has a necessary role in the embryonic, primary development process of SMC with consistent patterns being found in human GI diseased tissue.

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DNA methylation, through DNMT1, has an essential role in the development of gastrointestinal smooth muscle cells and disease [miRNA-Seq]

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DNA methylation, through DNMT1, has an essential role in the development of gastrointestinal smooth muscle cells and disease [RNA-Seq]

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DNA methylation, through DNMT1, has an essential role in the development of gastrointestinal smooth muscle cells and disease

Project description:DNA methylation, through DNMT1, has an essential role in the development of gastrointestinal smooth muscle cells and disease

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DNA methylation, through DNMT1, has an essential role in the development of gastrointestinal smooth muscle cells and disease [miRNA-Seq]

Project description:DNA methylation, through DNMT1, has an essential role in the development of gastrointestinal smooth muscle cells and disease [miRNA-Seq]

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DNA methylation, through DNMT1, has an essential role in the development of gastrointestinal smooth muscle cells and disease [RNA-Seq]

Project description:DNA methylation, through DNMT1, has an essential role in the development of gastrointestinal smooth muscle cells and disease [RNA-Seq]

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Whole-genome bisulfite sequencing of Dnmt1/3a/3b triple knockout (TKO) embryonic stem cells with or without expression of exogenous Dnmt1 before and after cell differentiation

Project description:Whole-genome bisulfite sequencing of Dnmt1/3a/3b triple knockout (TKO) embryonic stem cells with or without expression of exogenous Dnmt1 before and after cell differentiation.

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Dnmt1 has de novo activity targeted to transposable elements

Project description:DNA methylation plays a critical role in development, particularly in repressing retrotransposons. The mammalian methylation landscape is dependent on the combined activities of the canonical maintenance enzyme Dnmt1 and the de novo Dnmts, 3a and 3b. Here we demonstrate that Dnmt1 displays de novo methylation activity in vitro and in vivo with specific retrotransposon targeting. We used whole-genome bisulfite and long-read Nanopore sequencing in genetically engineered methylation depleted embryonic stem cells to provide an in-depth assessment and quantification of this activity. Utilizing additional knockout lines and molecular characterization, we show that Dnmt1's de novo methylation activity depends on Uhrf1 and its genomic recruitment overlaps with targets that enrich for Trim28 and H3K9 trimethylation. Our data demonstrate that Dnmt1 can de novo add and maintain DNA methylation, especially at retrotransposons and that this mechanism may provide additional stability for long-term repression and epigenetic propagation throughout development.

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Project description:DNA methylation is a key epigenetic modification involved in regulating gene expression and maintaining genomic integrity. Somatic patterns of DNA methylation are largely static, apart from focal dynamics at gene regulatory elements. To further advance our understanding of the role of DNA methylation in human development and disease, we inactivated all three catalytically active DNA methyltransferases in human embryonic stem cells (ESCs) using CRISPR/Cas9 genome editing. Disruption of DNMT3A or DNMT3B individually, as well as of both enzymes in tandem, creates viable, pluripotent cell lines with distinct effects on their DNA methylation landscape as assessed by whole-genome bisulfite sequencing. Surprisingly, in contrast to mouse, deletion of DNMT1 resulted in rapid cell death in human ESCs. To overcome the immediate lethality, we generated a doxycycline (DOX) responsive tTA-DNMT1* rescue line and readily obtained homozygous DNMT1 mutant lines. However, DOX-mediated repression of the exogenous DNMT1* initiates rapid, global loss of DNA methylation, followed by extensive cell death, demonstrating that DNA methylation is essential for human ESCs cultured in standard conditions. In summary, our data provide a comprehensive characterization of DNMT mutant ESCs, including single base genome-wide maps of their targets. RRBS methylation profiling of a time course of DNMT1* withdrawal in human ES cells

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Dnmt1 is essential to maintain progenitors in the perinatal intestinal epithelium.

Project description:We report that Dnmt1 is crucial during perinatal intestinal development. Loss of Dnmt1 in intervillus progenitor cells causes global hypomethylation, DNA damage, premature differentiation, and apoptosis, and consequently, loss of nascent villi. We further confirm the critical role for Dnmt1 during crypt development using the in vitro organoid culture system, and illustrate a clear differential requirement for Dnmt1 in immature versus mature organoids. These results demonstrate an essential role for Dnmt1 in maintaining genomic stability during intestinal development and the establishment of intestinal crypts.

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