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Dissecting developmental disorders caused by CTCF mutation at R567 [ChIP-seq]

ABSTRACT: In this study, CTCF ChIP experiments were performed to investigate the influence of CTCF mutation on its binding in mouse tissues.

ORGANISM(S): Mus musculus

PROVIDER: GSE214686 | GEO | 2024/05/06

REPOSITORIES: GEO

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Dissecting developmental disorders caused by CTCF mutation at R567 [Hi-C]

Project description:In this study, we performed BL-Hi-C experiments to investigate the influence of CTCF mutation on higher-order chromatin structures.

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Dissecting developmental disorders caused by CTCF mutation at R567

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

2024-05-05 | GSE214692 | GEO

Dissecting developmental disorders caused by CTCF mutation at R567 [4C]

Project description:In this study, we performed 4C sequencing experiments to investigate the change of chromatin interactions between the promoters of Pcdh genes and enhancers across cPcdh locus.

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Dissecting developmental disorders caused by CTCF mutation at R567 [SPARC-seq]

Project description:In this study, we performed SPARC-seq experiments in brain tissue from E18.5 mouse embryo.

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Dissecting developmental disorders caused by CTCF mutation at R567 [snRNA-seq]

Project description:In this study, we performed single nucleus RNA sequencing in heart, lung and cortex tissues from E18.5 mouse embryo.

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Dissecting developmental disorders caused by CTCF mutation at R567 [RNA-seq]

Project description:In this study, we analyzed gene expression change in brain tissues, in vitro cultured neurons and cortical organoids by using RNA-seq.

2024-05-06 | GSE214689 | GEO

CTCF mutation at R567 causes developmental disorders by 3D genome rearrangement, premature exhaustion of stem cells and abnormal neurodevelopment [scRNA-seq]

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ERCC1-XPF Cooperates with CTCF and the Cohesin to Facilitate the Developmental Silencing of Imprinted Genes

Project description:Inborn defects in DNA repairare associated with complex developmental disorders whose causal mechanisms are poorly understood. Using an in vivo biotinylation tagging approach in mice, we show that the nucleotide excision repair (NER) structure-specific endonuclease ERCC1-XPF complex interacts with the insulator binding protein CTCF, the cohesin subunits SMC1A and SMC3 and with MBD2; the factors co-localize with ATRX at the promoters and control regions (ICRs) of imprinted genes during postnatal hepatic development. Loss of Ercc1or exposure to mitomycin C triggers the localization of CTCF to heterochromatin, the dissociation of the CTCF-cohesin complex and ATRXfrom promoters and ICRs,altered histone marks and the aberrant developmental expression of imprinted genes without altering DNA methylation. We propose that ERCC1-XPF cooperates with CTCF and the cohesinto facilitatet he developmental silencing of imprinted genes and that persistent DNA damage triggers chromatin changes that affect gene expression programs associated with NER disorders.

2017-04-04 | PXD005897 | Pride

SNP array data for Wilms Tumor harboring de novo germline mutation in CTCF

Project description:SNP array was combined with next generation sequencing (NGS) to identify a unique de novo germline mutation in CTCF that became homozygous in the tumor. SNP array shows an LOH through chr16q where CTCF is located.

2022-01-11 | GSE193017 | GEO

Acute depletion of CTCF rewires genome-wide chromatin accessibility

Project description:The transcription factor CTCF appears indispensable in defining topologically associated domain boundaries and maintaining chromatin loop structures within these domains, supported by numerous functional studies. However, acute depletion of CTCF globally reduces chromatin interactions but does not significantly alter transcription. Here we systematically integrated multi-omics data including ATAC-seq, RNA-seq, WGBS, Hi-C, Cut&Run, CRISPR-Cas9 survival dropout screening, time-solved deep proteomic and phosphoproteomic analyses in cells carrying auxin-induced degron at endogenous CTCF locus. Acute CTCF protein degradation markedly rewired genome-wide chromatin accessibility. Increased accessible chromatin regions were largely located adjacent to CTCF-binding sites at promoter regions and insulator sites and were associated with enhanced transcription of nearby genes. In addition, we used CTCF-associated multi-omics data to establish a combinatorial data analysis pipeline to discover CTCF co-regulatory partners in regulating downstream gene expression. We successfully identified 40 candidates, including multiple established partners (i.e., MYC) supported by all layers of evidence. Interestingly, many CTCF co-regulators (e.g., YY1, ZBTB7A) that have evident alterations of respective downstream gene expression do not show changes at their expression levels across the multi-omics measurements upon acute CTCF loss, highlighting the strength of our system to discover hidden co-regulatory partners associated with CTCF-mediated transcription. This study highlights CTCF loss rewires genome-wide chromatin accessibility, which plays a critical role in transcriptional regulation

2021-07-04 | PXD026484 | Pride

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