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Acute depletion of CTCF directly affects MYC regulation through loss of enhancer–promoter looping

ABSTRACT: Acute depletion of CTCF directly affects MYC regulation through loss of enhancer–promoter looping

PROVIDER: PRJNA494510 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7958610_1.fastq.gz	Fastqsanger.gz
	SRR7958610_2.fastq.gz	Fastqsanger.gz
	SRR7958611_1.fastq.gz	Fastqsanger.gz
	SRR7958611_2.fastq.gz	Fastqsanger.gz
	SRR7958612_1.fastq.gz	Fastqsanger.gz

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Acute depletion of CTCF directly affects MYC regulation through loss of enhancer-promoter looping

Project description:Acute depletion of CTCF directly affects MYC regulation through loss of enhancer-promoter looping

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Acute depletion of CTCF directly affects MYC regulation through loss of enhancer–promoter looping

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Acute depletion of CTCF directly affects MYC regulation through loss of enhancer–promoter looping

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SuperSeries Acute depletion of CTCF directly affects MYC regulation through loss of enhancer–promoter looping

Project description:SuperSeries Acute depletion of CTCF directly affects MYC regulation through loss of enhancer–promoter looping

| PRJNA730431 | ENA

Acute depletion of CTCF directly affects MYC regulation through loss of enhancer-promoter looping.

Project description:Numerous pieces of evidence support the complex, 3D spatial organization of the genome dictates gene expression. CTCF is essential to define topologically associated domain boundaries and to facilitate the formation of insulated chromatin loop structures. To understand CTCF's direct role in global transcriptional regulation, we integrated the miniAID-mClover3 cassette to the endogenous CTCF locus in a human pediatric B-ALL cell line, SEM, and an immortal erythroid precursor cell line, HUDEP-2, to allow for acute depletion of CTCF protein by the auxin-inducible degron system. In SEM cells, CTCF loss notably disrupted intra-TAD loops and TAD integrity in concurrence with a reduction in CTCF-binding affinity, while showing no perturbation to nuclear compartment integrity. Strikingly, the overall effect of CTCF's loss on transcription was minimal. Whole transcriptome analysis showed hundreds of genes differentially expressed in CTCF-depleted cells, among which MYC and a number of MYC target genes were specifically downregulated. Mechanically, acute depletion of CTCF disrupted the direct interaction between the MYC promoter and its distal enhancer cluster residing ?1.8 Mb downstream. Notably, MYC expression was not profoundly affected upon CTCF loss in HUDEP-2 cells suggesting that CTCF could play a B-ALL cell line specific role in maintaining MYC expression.

| S-EPMC6648894 | biostudies-literature

Acute depletion of CTCF directly affects MYC regulation through loss of enhancer-promoter looping

Project description:In human cells, CTCF’s role in genomic organization and global transcription regulation is less clearly defined due to the lack of available tools to efficiently deplete CTCF. Here, we used an auxin-inducible degron system to conditionally deplete CTCF in a human B-cell lymphoblastic leukemia (B-ALL) cell line, SEM. Cut & Run ChIP-seq showed acute depletion of CTCF disrupted the direct interaction between the MYC promoter and its distal enhancer cluster residing ~1.8 Mb downstream.

2019-05-14 | GSE126619 | GEO

Acute depletion of CTCF directly affects MYC regulation through loss of enhancer–promoter looping

Project description:Myc is a family of regulator genes and proto-oncogenes that code for transcription factors. Gene expression of CTCF in human cancer cells and control uncover the disrupted enhancer-promoter regulation of MYC in human cancer cells.

2019-10-16 | GSE138862 | GEO

Acute depletion of CTCF directly affects MYC regulation through loss of enhancer–promoter looping

2019-05-14 | GSE121257 | GEO

Acute depletion of CTCF directly affects MYC regulation through loss of enhancer–promoter looping

2019-05-14 | GSE120781 | GEO

ZNF143 deletion alters enhancer/promoter looping and CTCF/cohesin geometry [HiChIP]

Project description:The transcription factor ZNF143 contains seven tandem zinc fingers and is involved in 3D genome construction; however, the mechanism by which ZNF143 functions in chromatin looping remains unclear. Here, we show that ZNF143 directionally recognizes diverse genomic sites and is required for chromatin looping between these sites. In addition, ZNF143 is located between CTCF and cohesin at numerous CTCF sites and ZNF143 removal narrows the space between CTCF and cohesin. Moreover, genetic deletion of ZNF143, in conjunction with acute CTCF depletion, revealed that ZNF143 and CTCF collaborate to regulate higher-order genome organization. Thus, ZNF143 is recruited by CTCF to the CTCF sites to regulate TAD formation and genome compartmentalization whereas directional recognition of DNA motifs directly by ZNF143 itself regulates promoter activity via chromatin looping.

2023-11-07 | GSE236635 | GEO

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