Similar Datasets
Project description:Genome-wide maps of CTCF in glioblastoma
| PRJNA579583 | ENA
Project description:We had performed the ATAC-seq in mouse and human glioblastoma stem cells to understand the epigenetic regulation of glioblastoma stem cells.
2022-03-20 | GSE163853 | GEO
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
Project description:We characterize H3K27ac and CTCF profiles of three primary glioblastoma cultures, and use them to bolster Hi-C datasets.
2019-06-06 | GSE121601 | GEO
Project description:Chromatin immunoprecipitation against CTCF followed by Illumina High-throughput sequencing. Examination of CTCF binding in red blood cells at 2 stages of development
2011-04-15 | E-GEOD-27945 | biostudies-arrayexpress
Project description:ChIP-seq based determination of CTCF binding sites in embryonic stem cells (ESC) Examination of CTCF binding sites
2011-05-19 | E-GEOD-25777 | biostudies-arrayexpress
Project description:While the elements encoding enhancers and promoters have been relatively well studied, the full spectrum of insulator elements which bind the CCCTC binding factor (CTCF), is relatively poorly characterised. In part, this is due the fact that their roles and activity is greatly influenced by their genomic context. Here we have developed an experimental system to determine the ability of consistently sized, individual CTCF elements to interpose between enhancers and promoters and thereby reduce gene expression during differentiation. Importantly each element is tested in the identical location thereby minimising the effect of genomic context. We found no correlation between the ability of CTCF elements to block enhancer-promoter activity with the amount of CTCF or cohesin bound at the natural genomic sites of these elements; the degree of evolutionary conservation; or their resemblance to the consensus core sequences. Nevertheless, we have shown that the strongest enhancer-promoter blockers include a previously described bound element lying upstream of the CTCF core motif. In addition, we found other uncharacterised DNAse1 footprints located close to the core sequence that may affect function. We have developed a high throughput assay of CTCF elements which will enable researchers to sub-classify CTCF elements in an unbiased way.
2023-08-12 | GSE240678 | GEO
Project description:CCCTC-binding factor (CTCF) is an architectural protein with context dependent functional outcomes. Although CTCF is conserved throughout Metazoan evolution, its functions have been only evaluated in a limited number of species. Here, we present the first analysis of CTCF binding in the zebrafish genome via chromatin immunoprecipitation followed by sequencing (ChIP-seq). To avoid the need of custom antibodies, we generated a transgenic line with an HA-tagged version of CTCF that enabled the identification of 37,625 CTCF peaks in 24 hours post-fertilization (hpf) embryos. We determined that CTCF peaks generally overlap with histone marks associated to enhancers and active promoters, and identified repeats that are enriched on CTCF binding sites. In addition, we show extended sites of CTCF binding as previously shown in mammals and lamprey, supporting the hypothesis of a CTCF “code” in vertebrates. Our results indicate a positive association between the abundance of CTCF at promoters and gene expression that could be explained by high DNA accessibility. Finally, analysis of chromosome conformation capture data confirms that histone marks associated with active chromatin are enriched at boundaries of topologically associating domains (TADs), but no general enrichment of CTCF peaks nor motifs is observed at these regions. Our zebrafish line and data generated will be important for future studies of genome organization aiming to characterize the roles of CTCF in non-mammalian vertebrates.
2020-03-30 | GSE133437 | GEO
Project description:Chromatin immunoprecipitation against CTCF followed by Illumina High-throughput sequencing. Examination of CTCF binding in embryonic stem cells and embryonic fibroblasts
2011-04-15 | E-GEOD-27944 | biostudies-arrayexpress
Project description:To understand how chromatin domains coordinate gene expression, we dissected select genetic elements organizing topology and transcription around the Prdm14 super enhancer in mouse embryonic stem cells. Taking advantage of allelic polymorphisms, we developed methods to sensitively analyze changes in chromatin topology, gene expression, and protein recruitment. We show that enhancer insulation does not strictly rely on loop formation between its flanking boundaries, that the enhancer activates the Slco5a1 gene beyond its prominent domain boundary, and that it recruits cohesin for loop extrusion. Upon boundary inversion, we find that oppositely-oriented CTCF terminates extrusion trajectories but does not stall cohesin, while deleted or mutated CTCF sites allow cohesin to extend its trajectory. Enhancer-mediated gene activation occurs independent of paused loop extrusion near the gene promoter. We expand upon the loop extrusion model to propose that cohesin loading and extrusion trajectories originating at an enhancer contribute to gene activation.
2021-06-30 | GSE173354 | GEO