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Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [ATAC-Seq]

ABSTRACT: Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [ATAC-Seq]

PROVIDER: PRJNA833072 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18963349_1.fastq.gz	Fastqsanger.gz
	SRR18963349_2.fastq.gz	Fastqsanger.gz
	SRR18963350_1.fastq.gz	Fastqsanger.gz
	SRR18963350_2.fastq.gz	Fastqsanger.gz
	SRR18963351_1.fastq.gz	Fastqsanger.gz

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Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4

Project description:Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4

| PRJNA833069 | ENA

Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [MNase-Seq]

Project description:Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [MNase-Seq]

| PRJNA833071 | ENA

Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [RNA-Seq]

Project description:Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [RNA-Seq]

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Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [ChIP-Seq]

Project description:Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [ChIP-Seq]

| PRJNA833074 | ENA

Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [RNA-Seq]

Project description:Transcription factors induce dynamic chromatin reorganization during cell fate transition. Pioneer transcription factors are defined as their capability to engage chromatin by binding to nucleosomal DNA in closed chromatin and inducing chromatin opening. However, it has been also shown that these activities are context dependent. Only a subset of pioneer factors’ binding sites become open and the rest of binding sites remain closed. The molecular mechanisms of this context dependent action are still largely unknown. Here, we explore dynamic chromatin rearrangement during GATA3 dependent mesenchymal-to-epithelial transition (MET) in breast cancer cells. We found site-specific kinetic differences in chromatin binding, nucleosome remodeling and chromatin opening by the pioneer factor GATA3. We also identified that a chromatin remodeling enzyme, CHD4, negatively regulates the GATA3-mediated chromatin opening. The silencing of CHD4 induces abnormal chromatin opening leading to unnecessary gene expression for MET. Our study suggests the active regulation of chromatin potential by the chromatin remodeling enzyme for successful cellular reprogramming.

2024-01-29 | GSE201798 | GEO

Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [ChIP-Seq]

2024-01-29 | GSE201797 | GEO

Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [MNase-Seq]

2024-01-29 | GSE201800 | GEO

Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4 [ATAC-Seq]

2024-01-29 | GSE201799 | GEO

Enhancer formation during cell reprogramming is edited by the chromatin remodeling factor CHD4

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

2024-01-29 | GSE201801 | GEO

CHD4 and the NuRD complex directly control cardiac sarcomere formation

Project description:Cardiac development relies on proper cardiomyocyte differentiation including expression and assembly of cell-type specific actomyosin subunits into a functional cardiac sarcomere. Control of this process involves not only promoting expression of cardiac sarcomere subunits but also repressing expression of non-cardiac myofibril paralogs. This level of transcriptional control requires broadly expressed multiprotein machines that modify and remodel the chromatin landscape to restrict transcription machinery access. Prominent among these is the Nucleosome Remodeling and Deacetylase (NuRD) complex, which includes the catalytic core subunit CHD4. Here, we demonstrate that direct CHD4-mediated repression of skeletal and smooth muscle myofibril isoforms is required for normal cardiac sarcomere formation, function, and embryonic survival early in gestation. Through transcriptomic and system genome-wide analyses of CHD4 localization, we identified novel CHD4 binding sites in smooth muscle myosin heavy chain, fast skeletal α-actin, and the fast skeletal troponin complex genes. We further demonstrate that in the absence of CHD4, cardiomyocytes in the developing heart form a hybrid muscle cell that contains cardiac, skeletal and smooth muscle myofibril components. These misexpressed paralogs intercalate into the nascent cardiac sarcomere to disrupt sarcomere formation and cause impaired cardiac function in utero. These results demonstrate the genomic and physiological requirements for CHD4 in mammalian cardiac development.

2018-05-15 | GSE109012 | GEO

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