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Mus musculus

ABSTRACT: CTCF functions as a chromatin insulator in the HoxA cluster during neurogenesis [4C-Seq]

PROVIDER: PRJNA257795 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1539371.fastq.gz	Fastqsanger.gz
	SRR1539372.fastq.gz	Fastqsanger.gz
	SRR1539373.fastq.gz	Fastqsanger.gz
	SRR1539374.fastq.gz	Fastqsanger.gz
	SRR1539375.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:CTCF functions as a chromatin insulator in the HoxA cluster during neurogenesis [RNA-Seq]

| PRJNA257793 | ENA

Mus musculus

Project description:CTCF functions as a chromatin insulator in the HoxA cluster during neurogenesis [ChIP-Seq]

| PRJNA257806 | ENA

Removable insulator facilitates higher-order chromatin remodeling and selective gene expression in the HOXA locus via the retinoic acid signaling [ChIP-chip]

Project description:Chromatin insulators partition the genome into the functional units to control gene expression especially in complex chromosomal regions. The CCCTC-binding factor (CTCF) is an insulator-binding protein which functions for transcriptional regulation and higher-order chromatin formation. Here we report that a removable CTCF insulator is responsible for the retinoic acid (RA)-mediated higher-order chromatin remodeling and selective gene expression in the human HOXA gene locus. Our detailed chromatin analyses characterized multiple CTCF-enriched sites and RA-responsive enhancers in this locus. These regulatory elements and transcriptionally silent HOXA genes were closely positioned under the basal condition. Notably, upon the RA signaling, the transcription factor RAR/RXR induced the loss of an adjacent CTCF binding and changed the higher-order chromatin conformation of the overall locus, establishing transcriptionally active, poised and repressive domains that were separated by stably localizing CTCF insulators. This study uncovers that removable insulator spatiotemporally switches higher-order chromatin and multiple gene activities at the chromosomal domain levels, via the cooperation of CTCF and key transcription factors.

2017-01-10 | GSE65930 | GEO

Removable insulator facilitates higher-order chromatin remodeling and selective gene expression in the HOXA locus via the retinoic acid signaling [ChIP-seq]

2017-01-10 | GSE80705 | GEO

Systematic assessment of ISWI subunits reveals that NURF creates local accessibility for proper CTCF function

Project description:Catalytic activity of the ISWI family of remodelers is critical for nucleosomal organization and transcription factor binding, including the insulator protein CTCF. To define which subcomplex mediates these diverse functions we phenotyped a panel of isogenic mouse stem cell lines each lacking one of six ISWI accessory subunits. Individual deletions of either CERF, RSF1, ACF, WICH or NoRC subcomplexes only moderately affect the chromatin landscape, while removal of the NURF-specific subunit BPTF leads to drastic reduction in chromatin accessibility and Snf2h ATPase localization around CTCF sites. While this reduces distances to the adjacent nucleosomes it only modestly impacts CTCF binding itself. In absence of accessibility, the insulator function of CTCF is nevertheless impaired resulting in lower occupancy of cohesin and cohesin-loading factors, and reduced insulation at these sites, highlighting the need of NURF-mediated remodeling for open chromatin and proper CTCF function. Our comprehensive analysis reveals a specific role for NURF in mediating Snf2h localization and chromatin opening at bound CTCF sites showing that local accessibility is critical for cohesin binding and insulator function.

2024-03-13 | PXD042945 | Pride

A CTCF binding element regulates RA-induced early ESCs differentiation through orchestrating long-range chromatin interactions between its adjacent enhancers and HoxA

Project description:Proper Homeobox A (HoxA) cluster genes expression is essential for embryonic stem cells (ESCs) differentiation and individual development. However, the mechanisms controlling the precise spatiotemporal expression of HoxA cluster genes during early ESCs differentiation remain largely unknown. Here, we find a CTCF binding element (CBE+47kb) closest to the 3'-end of HoxA locus within a topologically associated domains (TAD) in ESCs. CRISPR-Cas9 mediated the CBE+47kb knockout significantly promotes expression of HoxA cluster genes and early ESCs differentiation induced by RA compared with wild type cells. In mechanism, we found that there was a significant differently long-range chromatin interactions between its adjacent enhancers and HoxA in CBE+47kb knockout cells through chromosome conformation capture assay (Capture-C), indicating that CBE+47kb can precisely organize interactions between its adjacent enhancers and HoxA chromatins. Furthermore, we also showed that its adjacent enhancers deletion shows significantly synthetic inhibition effect on HoxA genes expression, suggesting that these enhancers are required for RA-induced HoxA genes expression. Our study reveals that a new functional CBE+47 can regulate HoxA genes expression through orchestrating long-range chromatin interactions between its adjacent enhancers and HoxA, thus maintaining RA-induced early ESCs proper differentiation.

2020-07-16 | GSE154495 | GEO

CTCF boundary remodels chromatin domain and drives aberrant HOX gene transcription in acute myeloid leukemia

Project description:We analyzed RNA-seq, ATAC-seq, ChIP-seq and 4C-seq data to find that CTCF binding site located between HOXA7 and HOXA9 genes (CBS7/9) is critical for establishing and maintaining aberrant HOXA9-HOXA13 gene expression in AML. Disruption of the CBS7/9 boundary resulted in spreading of repressive H3K27me3 into the posterior active HOXA chromatin domain that subsequently impaired enhancer/promoter chromatin accessibility and disrupted ectopic long-range interactions among the posterior HOXA genes. Consistent with the role of the CBS7/9 boundary in HOXA locus chromatin organization, attenuation of the CBS7/9 boundary function reduced posterior HOTTIP lincRNA and HOXA gene expression and altered myeloid specific transcriptome profiles important for pathogenesis of myeloid malignancies.

2018-05-17 | GSE113191 | GEO

CRISPR and biochemical screens Identify MAZ as a co-factor in CTCF-mediated insulation at Hox Clusters [4C-seq_set2]

Project description:In this experiment, we sought to identify how topological organization changes at HoxA cluster in WT, MAZ HoxA(Δ5|6) and CTCF (Δ5|6:6|7) cells during differentiation of mouse embryonic stem cells (ESCs) into cervical motor neurons (MNs).

2022-02-06 | GSE190988 | GEO

Mediation of CTCF transcriptional insulation by DEAD-box RNA-binding protein p68 and steroid receptor RNA activator SRA

Project description:CCCTC-binding factor (CTCF) is a DNA-binding protein that plays important roles in chromatin organization, though the mechanism by which CTCF carries out these functions is not fully understood. Recent studies show that CTCF recruits the cohesin complex to insulator sites and that cohesin is required for insulator activity. Here we have shown that the DEAD box RNA helicase p68 (DDX5) and its associated noncoding RNA, steroid receptor RNA activator (SRA), form a complex with CTCF that is essential for insulator function. p68 was detected at CTCF sites in the IGF2/H19 imprinted control region (ICR) as well as other genomic CTCF sites. In vivo depletion of SRA or p68 reduced CTCF-mediated insulator activity at the IGF2/H19 ICR, increased levels of IGF2 expression, and increased interactions between the endodermal enhancer and IGF2 promoter. p68/SRA also interacts with members of the cohesin complex. Depletion of either p68 or SRA does not affect CTCF binding to its genomic sites, but it does reduce cohesin binding. The results suggest that p68/SRA stabilizes the interaction of cohesin with CTCF, by binding to both, and is required for proper insulator function. Identification of p68-binding sites in Hela cells using ChIP-Seq.

2010-11-16 | E-GEOD-24126 | biostudies-arrayexpress

Mus musculus

Project description:CTCF binding polarity determines chromatin looping [4C]

| PRJNA294301 | ENA