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Genome-wide identification of CTCF and Cohesin binding sites in neonatal mouse brain

ABSTRACT: ChIP-seq for CTCF and Rad21 in 3 week old mouse brain from reciprocal BxC and CxB crosses. One biological replicate of each.

ORGANISM(S): Mus musculus

PROVIDER: GSE35140 | GEO | 2013/06/20

SECONDARY ACCESSION(S): PRJNA150703

REPOSITORIES: GEO

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Genome-wide identification of CTCF and Cohesin binding sites in neonatal mouse brain

Project description:ChIP-seq for CTCF and Rad21 in 3 week old mouse brain from reciprocal BxC and CxB crosses. One biological replicate of each. Examination of CTCF and Cohesin binding sites in neonetal mouse brain

2013-06-20 | E-GEOD-35140 | biostudies-arrayexpress

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ChIP-seq data in mESCs show ZFP661 suppresses cohesin binding at CTCF barriers

Project description:In this assay, we aimed to investigate the occupancy of ZFP661 in the mouse genome and its possible role in regulating the occupancies of CTCF and cohesin, which are two key factors in establishing 3D chromatin structures. To achieve this, we performed ChIP-seq in ZFP661-3HA endogenously tagged mESCs (for ZFP661), Zfp661 knockout (KO) mESCs (for CTCF and RAD21), and ZFP661-3HA overexpressing (OE) mESCs (for ZFP661, CTCF, RAD21, KAP1, and H3K9me3). Our results reveal that 1) ZFP661 binding peaks were co-occupied with those of CTCF; 2) ZFP661 binds exclusively inside the CTCF loop anchors; and 3) ZFP661 can suppress cohesin binding at CTCF barriers without altering CTCF binding.

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Project description:Sequencing files provided here include mouse liver ChIP-seq for CTCF and the cohesin subunit Rad21. These files are part of a larger study ("CTCF and Cohesin link sex-biased distal regulatory elements to sex-biased gene expression in mouse liver") where we compare CTCF and cohesin binding in male and female mouse liver as well as differences in chromatin conformation (DNA looping).

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ChIP-seq analyses of CTCF binding in liver samples from CAST/EiJ and SPRET/EiJ (Mus spretus) mice, and of the cohesin subunit RAD21 in C57BL/6J mouse liver

Project description:We explored the relationship between the evolutionary dynamics of CTCF binding and the functional stability of higher order genome structures, by performing ChIP-seq experiments in closely related Mus species or strains and intersecting with Hi-C-derived topologically associating domains (TADs) and expression data. All experiments were performed in adult male liver samples in 3 biological replicates and with an input control set. We also generated RAD21 (cohesin subunit) ChIP-seq from a replicate of adult male mouse (C57BL/6J) liver to determine localization of cohesin with respect to CTCF.

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CTCF and cohesin regulate chromatin loop stability with distinct dynamics

Project description:The study investigates the nuclear organization and the binding dynamics of CTCF and cohesin by super-resolution microscopy and ChIP-seq. We determined the genome-wide binding profile of CTCF and Rad21 cohesin subunit in wild type mouse ES cells and compared them to a double FLAG-Halo-mCTCF/mRad21-SNAPf-V5 knock-in mES line, generated by CRISPR/Cas9-mediated genome editing to perform imaging experiments.

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CTCF/cohesin-binding sites are frequently mutated in cancer

Project description:Cohesin is present in almost all active enhancer regions, where it is associated with transcription factors. Cohesin frequently colocalizes with CTCF (CCCTC-binding factor), affecting genomic stability, expression and epigenetic homeostasis. Cohesin subunits are mutated in cancer, but CTCF/cohesin-binding sites (CBSs) in DNA have not been examined for mutations. Here we report frequent mutations at CBSs in cancers displaying a mutational signature where mutations in A•T base pairs predominate. Integration of whole-genome sequencing data from 213 colorectal cancer (CRC) samples and chromatin immunoprecipitation sequencing (ChIP-exo) data identified frequent point mutations at CBSs. In contrast, CRCs showing an ultramutator phenotype caused by defects in the exonuclease domain of DNA polymerase ɛ (POLE) displayed significantly fewer mutations at and adjacent to CBSs. Analysis of public data showed that multiple cancer types accumulate CBS mutations. CBSs are a major mutational hotspot in the noncoding cancer genome.

| EGAS00001003010 | EGA

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