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Tunable DNMT1 degradation reveals cooperation of DNMT1 and DNMT3B in regulating DNA methylation dynamics and genome organization (ChIP-Seq).

ABSTRACT: Tunable DNMT1 degradation reveals cooperation of DNMT1 and DNMT3B in regulating DNA methylation dynamics and genome organization (ChIP-Seq).

PROVIDER: PRJNA1055943 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27330846_1.fastq.gz	Fastqsanger.gz
	SRR27330846_2.fastq.gz	Fastqsanger.gz
	SRR27330847_1.fastq.gz	Fastqsanger.gz
	SRR27330847_2.fastq.gz	Fastqsanger.gz
	SRR27330848_1.fastq.gz	Fastqsanger.gz

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Tunable DNMT1 degradation reveals cooperation of DNMT1 and DNMT3B in regulating DNA methylation dynamics and genome organization

Project description:Tunable DNMT1 degradation reveals cooperation of DNMT1 and DNMT3B in regulating DNA methylation dynamics and genome organization

| PRJNA1055937 | ENA

Tunable DNMT1 degradation reveals cooperation of DNMT1 and DNMT3B in regulating DNA methylation dynamics and genome organization (Hi-C).

Project description:Tunable DNMT1 degradation reveals cooperation of DNMT1 and DNMT3B in regulating DNA methylation dynamics and genome organization (Hi-C).

| PRJNA1055944 | ENA

Tunable DNMT1 degradation reveals cooperation of DNMT1 and DNMT3B in regulating DNA methylation dynamics and genome organization (Hi-C).

Project description:DNA methylation (DNAme) is a key epigenetic mark that regulates critical biological processes maintaining overall genome stability. Given its pleiotropic function, studies of DNAme dynamics are crucial, but currently available tools to interfere with DNAme have limitations and major cytotoxic side effects. Here, we present cell models that allow inducible and reversible DNAme modulation through DNMT1 depletion. By dynamically assessing whole genome and locus-specific effects of induced passive demethylation through cell divisions, we reveal a cooperative activity between DNMT1 and DNMT3B, but not of DNMT3A, to maintain and control DNAme. We show that gradual loss of DNAme is accompanied by progressive and reversible changes in heterochromatin, compartmentalization, and peripheral localization. DNA methylation loss coincided with a gradual reduction of cell fitness due to G1 arrest, but with minor level of mitotic failure. Altogether, this system allows DNMTs and DNA methylation studies with fine temporal resolution, which may help to reveal the etiologic link between DNAme dysfunction and human disease.

2024-02-01 | GSE251934 | GEO

Tunable DNMT1 degradation reveals cooperation of DNMT1 and DNMT3B in regulating DNA methylation dynamics and genome organization (ChIP-Seq).

2024-02-01 | GSE251932 | GEO

Tunable DNMT1 degradation reveals DNMT1/DNMT3B synergy in DNA methylation and genome organization.

Project description:DNA methylation (DNAme) is a key epigenetic mark that regulates critical biological processes maintaining overall genome stability. Given its pleiotropic function, studies of DNAme dynamics are crucial, but currently available tools to interfere with DNAme have limitations and major cytotoxic side effects. Here, we present cell models that allow inducible and reversible DNAme modulation through DNMT1 depletion. By dynamically assessing whole genome and locus-specific effects of induced passive demethylation through cell divisions, we reveal a cooperative activity between DNMT1 and DNMT3B, but not of DNMT3A, to maintain and control DNAme. We show that gradual loss of DNAme is accompanied by progressive and reversible changes in heterochromatin, compartmentalization, and peripheral localization. DNA methylation loss coincides with a gradual reduction of cell fitness due to G1 arrest, with minor levels of mitotic failure. Altogether, this system allows DNMTs and DNA methylation studies with fine temporal resolution, which may help to reveal the etiologic link between DNAme dysfunction and human disease.

| S-EPMC10876481 | biostudies-literature

Tunable DNMT1 degradation reveals cooperation of DNMT1 and DNMT3B in regulating DNA methylation dynamics and genome organization

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

2024-02-01 | GSE251935 | GEO

Effect of depletion of UHRF1, DNMT1, DNMT3B during differentiation

Project description:To investigate gene regulation by UHRF1, DNMT1, DNMT3B in THP-1 cells during differentiation, we established stable knockdown THP-1 cell lines.

2022-06-25 | GSE206742 | GEO

Gene expression profile of Dnmt1 flox/flox, Dnmt3a flox/flox, Dnmt3b flox/flox, cre negative (Wild type) and Dnmt1 flox/flox, Dnmt3a flox/flox, Dnmt3b flox/flox, Rx-cre (Triple mutant) murine retina transcriptomes

Project description:Purpose: The goal of this study was to identify the gene expression profile of mouse retina which carries deletions in Dnmt1, Dnmt3a and Dnmt3b genes. Method: Retinal mRNA profiles of Postnatal day 15 wild type mice and Dnmt1, Dnmt3a and Dnmt3b mutant mice were generated by deep-sequencing

2016-11-28 | GSE81191 | GEO

Effect of depletion of UHRF1, DNMT1, DNMT3B during differentiation

Project description:Effect of depletion of UHRF1, DNMT1, DNMT3B during differentiation

| PRJNA851905 | ENA

Targeted disruption of DNMT1, 3A and 3B in human embryonic stem cells [DNMT1]

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

2015-03-30 | E-GEOD-63279 | biostudies-arrayexpress

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