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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE214688 | GEO | 2024/05/06

REPOSITORIES: GEO

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Dissecting developmental disorders caused by CTCF mutation at R567

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

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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 [ChIP-seq]

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

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

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

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Project description:We performed 4C-seq to measure the chromatin contact changes between Pcdh-b and their enhancers, HS18-20.

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Project description:4C contact profiles of the Pcdh-b enhancers HS18-20

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

Project description:In this study, we performed single RNA sequencing in 1-month and 2-month cortical organoids derived from wild-type and Ctcf heterozygous hESCs.

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