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CTCF ChIP-MS from crosslinked chromatin in mouse embryonic stem cells (mESCs) and motor neurons (MNs)

ABSTRACT: To identify CTCF partners and co-localizing proteins from crosslinked chromatin in mESCs and MNs in endogenous conditions. The goal is to identify proteins within each sample with respect to wild-type control for each.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Motor Neuron, Cell Culture, Embryonic Stem Cell

SUBMITTER: Havva Ortabozkoyun Kara

LAB HEAD: Danny Reinberg

PROVIDER: PXD030543 | Pride | 2022-02-15

REPOSITORIES: Pride

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	QE04236-2.raw	Raw
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	QE04237-2.raw	Raw
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Publications

CRISPR and biochemical screens identify MAZ as a cofactor in CTCF-mediated insulation at Hox clusters.

Ortabozkoyun Havva H Huang Pin-Yao PY Cho Hyunwoo H Narendra Varun V LeRoy Gary G Gonzalez-Buendia Edgar E Skok Jane A JA Tsirigos Aristotelis A Mazzoni Esteban O EO Reinberg Danny D

Nature genetics 20220210 2

CCCTC-binding factor (CTCF) is critical to three-dimensional genome organization. Upon differentiation, CTCF insulates active and repressed genes within Hox gene clusters. We conducted a genome-wide CRISPR knockout (KO) screen to identify genes required for CTCF-boundary activity at the HoxA cluster, complemented by biochemical approaches. Among the candidates, we identified Myc-associated zinc-finger protein (MAZ) as a cofactor in CTCF insulation. MAZ colocalizes with CTCF at chromatin borders ...[more]

PMID: 35145304

Similar Datasets

CTCF ChIP-MS from native chromatin in mouse embryonic stem cells (mESCs) and motor neurons (MNs)

Project description:To identify CTCF partners and co-localizing proteins from native chromatin in mESCs and MNs in endogenous conditions. The goal is to identify proteins within each sample with respect to wild-type control for each.

2022-02-11 | PXD030452 | Pride

Molecular profiling of Ctcf hemizygous mouse embryonic fibroblasts: HiC

Project description:CTCF is a highly conserved and ubiquitously expressed protein involved in several fundamental processes such as fine-tuning gene expression, imprinting, X-chromosome inactivation and 3D chromatin organisation. To understand the impact of differences in the concentration of CTCF abundance on these processes, we exploit a CTCF hemizygous mouse model with a stable reduction in the concentration of this protein. We derived independent primary lines of mouse embryonic fibroblasts (MEFs) from wildtype and CTCF-hemizygous mouse E13.5 embryos. For three biological replicates, cells were fixed in DMEM containing 2% fresh formaldehyde and incubated at room temperature for 10 min, quenched with 1M glycine for 5 min, and washed twice with ice cold PBS, before being flash-frozen at -80°C. Cross-linked cells were lysed, followed by chromatin HindIII digestion, biotinylataion, ligation, proteinase K treatment, DNA purification, sonication, end repair, biotin pull-down, adapter ligation, and PCR amplification. Pooled indexed libraries were sequenced on an Illumina HiSeq4000 to produce paired-end 150bp reads. On the same MEF lines we have performed RNAseq and ChIPseq for CTCF, H3K4me3 and H3K27ac.

2018-07-29 | E-MTAB-6262 | biostudies-arrayexpress

CTCF loss has limited effects on genome architecture in Drosophila despite critical regulatory functions.

Project description:Proteins co-purifying with recombinantly purified and N-terminally GFP-3C-tagged CTCF N-terminus (amino acids 1-293) produced in bacteria were identified by incubating the tagged bait with soluble nuclear protein extracts from 0-12h hour-old wildtype (OregonR strain) Drosophila melanogaster embryos.

2021-01-18 | PXD019487 | Pride

CTCF cooperates with CtIP to drive homologous recombination repair of double-strand breaks

Project description:The pleiotropic CCCTC-binding factor (CTCF) plays a role in homologous recombination (HR) repair of DNA double-strand breaks (DSBs). However, the precise mechanistic role of CTCF in HR remains largely unclear. Here, we show that CTCF engages in DNA end resection, which is the initial, crucial step in HR, through its interactions with MRE11 and CtIP. Depletion of CTCF profoundly impairs HR and attenuates CtIP recruitment at DSBs. CTCF physically interacts with MRE11 and CtIP and promotes CtIP recruitment to sites of DNA damage. Subsequently, CTCF facilitates DNA end resection to allow HR, in conjunction with MRE11-CtIP. Notably, the zinc finger domain of CTCF binds to both MRE11 and CtIP and enables proficient CtIP recruitment, DNA end resection, and HR. The N-terminus of CTCF is able to bind to only MRE11 and its C-terminus is incapable of binding to MRE11 and CtIP, thereby resulting in compromised CtIP recruitment, DSB resection, and HR. Overall, this suggests an important function of CTCF in DNA end resection through the recruitment of CtIP at DSBs. Collectively, our findings identify a critical role of CTCF at the first control point in selecting the HR repair pathway

2019-11-12 | PXD014441 | Pride

The epigenetic pattern and genome-wide CTCF occupancy in HL-60 cells treated with ATRA

Project description:10^7 HL-60 cells were treated with 10 uM ATRA for two and five days. 10% whole cell lysates were saved as input after genomic DNA was broken into 200-500 bp by sonication. 1 μg IP grade antibodies of CTCF, H3K4me3 or H3K27me3 (CST, Boston, USA) were incubated with the rest of the lysate overnight, followed by 2 h protein-A beads incubation at 4 °C for target protein pull down. The CTCF enriched or H3K4/27me3 modified DNA or input DNA were repaired to 3’-dA overhang and added the ligated adapter. The DNA library was eliminated the unligated adapters and selected the appropriate size for sequence using an Illumina X Ten platform. The raw sequence reads of input and IP were trimmed adaptors and filter out low quality reads using Cutadapt (v1.9.1) and Trimmomatic (v0.35), and checked the quality of clean reads using Fastqc. Next, clean reads were mapped to the human genome (assembly hg38) using the Bowtie 2 (v2.2.6) algorithm. The process of peak calling (p<0.01) were performed by MACS 2 (v2.1.1) and analyzed the different binding domains based on FDR value less than 0.05 and annotated by DiffBind. De novo motif were analyzed using the R language and MEME. The peaks on certain genomic loci were visualized by Integrative Genomics Viewer (IGV). Gene ontology (GO) Analysis was used to interpret the biological function of the genes associated with differential peaks.

2020-05-07 | E-MTAB-8558 | biostudies-arrayexpress

CTCF binding in B cells and Plasmablasts

Project description:The mammalian CCCTC-binding factor (CTCF) regulates gene expression through the formation of higher order chromatin structures. Recent evidence has implicated a role for CTCF in regulating gene expression in the human MHCII locus. To investigate the role of CTCF in murine MHCII gene expression we mapped CTCF binding sites in B cells (MHCII+ cells) and Plasmablasts which are differentiated B cells that have silenced MHCII gene expression. These observations lead to the identification of differential CTCF binding during differentiation in these cell types and suggest mechanims of MHCII gene regulation. Comparison of CTCF binding in B cells and Plasmablasts in mice using ChIP-seq

2014-02-05 | E-GEOD-44637 | biostudies-arrayexpress

CTCF demarcates chromatin domains

Project description:Insulators are DNA elements, which prevent inappropriate interactions between the neighboring regions of the genome. They can be functionally classified as either enhancer blockers or domain barriers. CTCF (CCCTC binding factor) is the only known major insulator binding protein in the vertebrates and has been shown to bind many enhancer-blocking elements. However, it is not clear whether it plays a role in chromatin domain barriers between active and repressive domains. Here, we used ChIP-Seq to map the genome-wide binding sites of CTCF in three cell types and identified significant binding of CTCF to the boundaries of repressive chromatin domains marked by H3K27me3. Although we find an extensive overlapping of CTCF binding sites across the three cell types, its association with the domain boundaries is cell type-specific. We further show that the nucleosomes flanking CTCF binding sites are well positioned and associated with histone H2AK5 acetylation (H2AK5ac). Interestingly, we found a complementary pattern between the repressive H3K27me3 and the active H2AK5ac regions, which are separated by CTCF. Our findings indicate that CTCF may play important roles in the barrier activity of insulators and provide a resource for further investigation of the CTCF function in organizing chromatin in the human genome. Examination of the role of CTCF in chromatin domain barrier function In addition to the ChIP-seq analysis, two replicates of HeLa expression data were studied.

2008-10-20 | E-GEOD-12889 | biostudies-arrayexpress

Female-specific CTCF binding on the inactive X chromosome in mouse

Project description:In mammals, genes located on the X chromosome are present in one copy in XY males and two in XX females. To balance the dosage of X-linked gene expression between the sexes one of the two X chromosomes in females is silenced by X inactivation initiated by up-regulation of the lncRNA (long non-coding RNA) Xist and recruitment of specific chromatin modifiers for silencing. The inactivated X chromosome becomes heterochromatic and visits a specific nuclear compartment adjacent to the nucleolus. We report a novel role for the X-linked lncRNA Firre in anchoring the inactive mouse X chromosome and preserving one of its main epigenetic features, trimethylation of histone H3 at lysine 27 (H3K27me3). Similar to Dxz4, Firre is expressed from a macrosatellite repeat locus associated with a cluster of CTCF and cohesin binding specifically on the inactive X. CTCF binding initially present in both male and female mouse embryonic stem cells was found to be lost from the active X during development. The Firre and Dxz4 loci on the inactive X were preferentially located adjacent to the nucleolus. Knockdown of Firre RNA disrupted perinucleolar targeting and H3K27me3 levels in mouse fibroblasts, demonstrating an important role for this lncRNA in maintenance of one of the main epigenetic features of the X chromosome. There was no X-linked gene reactivation after Firre knockdown; however, a compensatory increase in the expression of chromatin modifier genes implicated in X silencing was observed. In female ES cells Firre RNA knockdown did not disrupt Xist expression/coating nor silencing of G6pdx during differentiation, suggesting that Firre does not play a role in the onset of X inactivation. We conclude that the X-linked lncRNA Firre helps position the inactive X chromosome near the nucleolus and preserve one of its main epigenetic features. Examination of allelic protein-binding or histone modification profiles in Patski cells.

2015-02-26 | E-GEOD-66262 | biostudies-arrayexpress

Evolutionary comparison of CTCF and YY1 binding in primate lymphoblastoid cell lines

Project description:We performed an evolutionary comparison of the binding of the TF CTCF in human, chimpanzee, gorilla, orang-utan, macaque, baboon and marmoset using lymphoblastoid cell lines (LCLs). We also probes YY1 binding in human, chimpanzee, orang-utan and baboon LCLs as well as human and mouse liver.

2013-11-20 | E-MTAB-1511 | biostudies-arrayexpress

De novo mutations in the genome organizer CTCF cause Intellectual Disability (ChIP-Seq)

Project description:An increasing number of genes involved in chromatin structure and epigenetic regulation has been implicated in a variety of developmental disorders, often including intellectual disability. By trio exome sequencing and subsequent mutational screening we now identified two de novo frameshift mutations and one de novo missense mutation in the CTCF gene in individuals with intellectual disability, microcephaly and growth retardation. Furthermore, a patient with a larger deletion including CTCF was identified. CTCF (CCCTC-binding factor) is one of the most important chromatin organizers in vertebrates and is involved in various chromatin regulation processes such as higher order of chromatin organization, enhancer function, and maintenance of three-dimensional chromatin structure. Transcriptome analyses in all three patients with point mutations revealed deregulation of genes involved in signal transduction and emphasized the role of CTCF in enhancer-driven expression of genes. Our findings indicate that haploinsufficiency of CTCF affects genomic interaction of enhancers and their regulated gene promoters that drive developmental processes and cognition. ChIP-seq analysis of CTCF genomic binding sites in lymphocytes of a control individual (no replicates).

2013-06-01 | E-GEOD-46832 | biostudies-arrayexpress

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