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Gibbin drives epithelial development by toggling CTCF binding and DNA methylation

ABSTRACT: Gibbin drives epithelial development by toggling CTCF binding and DNA methylation

PROVIDER: PRJNA687497 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13294968_1.fastq.gz	Fastqsanger.gz
	SRR13294968_2.fastq.gz	Fastqsanger.gz
	SRR13294969_1.fastq.gz	Fastqsanger.gz
	SRR13294969_2.fastq.gz	Fastqsanger.gz
	SRR13294970_1.fastq.gz	Fastqsanger.gz

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Gibbin drives epithelial development by toggling CTCF binding and DNA methylation

Project description:The goal of these ATAC-seq experiments was to determine changes in chromatin accesiblity caused by loss of Gibbin (AHDC1) or GATA3 in non-neural ectoderm.

2022-02-13 | GSE163769 | GEO

The Xia-Gibbs Syndrome protein Gibbin regulates mesodermal DNA methylation to pattern epithelial development (ChIP-Seq)

Project description:The goal of these ChIP-seq experiments was to determine binding sites for AHDC1/Gibbin, GATA3, CTCF proteins or the H3K9me3 histone mark in cells treated with RA/BMP4.e

2022-02-13 | GSE180492 | GEO

The Xia-Gibbs Syndrome protein Gibbin regulates mesodermal DNA methylation to pattern epithelial development (HiChIP)

Project description:The goal of these Hi-ChIP experiments was to determine changes in cohesin-mediated chromatin contacts caused by AHDC1/Gibbin knockout.

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The Xia-Gibbs Syndrome protein Gibbin regulates mesodermal DNA methylation to pattern epithelial development (RNA-Seq)

Project description:The goal of these RNA-seq experiments was to determine changes in gene expression caused by loss of Gibbin (AHDC1) or GATA3 at various time points following addition of RA/BMP4.

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Gibbin (AHDC1) mesodermal regulation controls epithelial patterning

Project description:Gibbin (AHDC1) mesodermal regulation controls epithelial patterning

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Gibbin (AHDC1) regulates the mesoderm to pattern epithelial development

Project description:Gibbin (AHDC1) regulates the mesoderm to pattern epithelial development

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Low affinity CTCF binding drives transcriptional regulation whereas high affinity binding encompasses architectural functions.

Project description:Low affinity CTCF binding drives transcriptional regulation whereas high affinity binding encompasses architectural functions.

| PRJNA856492 | ENA

Low affinity CTCF binding drives transcriptional regulation whereas high affinity binding encompasses architectural functions.

Project description:This SuperSeries is composed of the SubSeries listed below. CTCF is a DNA-binding protein which plays critical roles in chromatin structure organization and transcriptional regulation; however, little is known about the functional determinants of different CTCF binding sites (CBS). Using a conditional mouse model, we have identified one set of CBSs that are lost upon CTCF depletion (lost CBSs) and another set that persists (retained CBSs). Retained CBSs are more similar to the consensus CTCF binding sequence and usually span tandem CTCF peaks. Lost CBSs are enriched at enhancers and promoters and associate with active chromatin marks and higher transcriptional activity. In contrast, retained CBSs are enriched at TAD and loop boundaries. Integration of ChIP-seq and RNA-seq data has revealed that retained CBSs are located at the boundaries between distinct chromatin states, acting as chromatin barriers. Our results provide evidence that transient, lost CBSs are involved in transcriptional regulation, whereas retained CBSs are critical for establishing higher-order chromatin architecture.

2023-02-10 | GSE207640 | GEO

CTCF binding polarity determines chromatin looping [4C]

Project description:CCCTC-binding factor (CTCF) is an architectural protein involved in the three-dimensional organization of chromatin. In this study, we systematically assayed the 3D genomic contact profiles of hundreds of CTCF binding sites in multiple tissues with high-resolution 4C-seq. We find both developmentally stable and dynamic chromatin loops. As recently reported, our data also suggest that chromatin loops preferentially form between CTCF binding sites oriented in a convergent manner. To directly test this, we used CRISPR-Cas9 genome editing to delete core CTCF binding sites in three loci, including the CTCF site in the Sox2 super-enhancer. In all instances, CTCF and cohesin recruitment were lost, and chromatin loops with distal CTCF sites were disrupted or destabilized. Re-insertion of oppositely oriented CTCF recognition sequences restored CTCF and cohesin recruitment, but did not re-establish chromatin loops. We conclude that CTCF binding polarity plays a functional role in the formation of higher order chromatin structure. 4C-seq was performed on a large number of viewpoints in E14 embryonic stem cells, neural precursor cells and primary fetal liver cells

2015-10-29 | E-GEOD-72539 | biostudies-arrayexpress

CTCF binding in gorilla

Project description:CTCF binding in gorilla

| PRJEB2540 | ENA