ChIP-Seq analysis of CCCTC-binding factor (CTCF) binding in rodents
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB21041 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1992800_1.fastq.gz | Fastqsanger.gz | |||
| ERR1992800_2.fastq.gz | Fastqsanger.gz | |||
| ERR1992801_1.fastq.gz | Fastqsanger.gz | |||
| ERR1992801_2.fastq.gz | Fastqsanger.gz | |||
| ERR1992802_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:We explored the microevolutionary trends of CTCF binding evolution by preforming ChIP-seq experiments in five closely related Mus strains, subspecies and species: Mus musculus domesticus, Mus musculus castaneus, Mus spretus, Mus caroli and Mus pahari. All experiments were performed in adult male liver samples in 3 biological replicates and with an input control set. Complementary RNA-seq data from this same study have been deposited in ArrayExpress under accession numebr E-MTAB-5768 ( https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-5768 ).
2018-03-06 | E-MTAB-5769 | biostudies-arrayexpress
Project description:ChIP-seq analysis of CCCTC-binding factor (CTCF) binding in livers of C3H mice
| PRJEB54882 | ENA
Project description:Chromosome segregation in mitosis and meiosis depends on sister chromatid cohesion mediated by cohesin complexes. Mutation of cohesin and other cohesion proteins causes transcriptional and developmental defects in animals and humans, but the molecular cause of these phenotypes is unknown. Here we describe 8811 cohesin binding sites in the human genome and show that the CCCTC-binding factor (CTCF) is associated with 88% of these. CTCF is dispensable for loading of cohesin onto DNA but is required for enrichment of cohesin at its binding sites. We provide evidence that cohesin is required for the role of CTCF sites in insulating promoters from distant enhancers. Like CTCF, cohesin is located on the maternal but not on the paternal allele of the H19 imprinting control region (ICR) and is required for imprinting of the H19-Igf2 locus. We find that cohesin is widely expressed in mammalian tissues, consistent with a cohesionindependent role in regulating gene expression. We propose that cohesin functions as a transcriptional insulator and speculate that subtle deficiencies in this function may be the cause of "cohesinopathies" such as Cornelia de Lange and Roberts syndrome. Keywords: ChIP-chip analysis
2008-01-30 | GSE9613 | GEO
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
Project description:The transcription factor CCCTC-binding factor (CTCF) modulates pleiotropic functions mostly related to gene expression regulation. The role of CTCF in large scale genome organization is also well established. A unifying model to explain relationships between many CTCF-mediated activities involve direct or indirect interactions with numerous protein cofactors recruited to specific binding sites. The co-association of CTCF with other architectural proteins such as cohesin, chromodomain helicases and BRG1 further support the interplay between master regulators of mammalian genome folding. Here we report a comprehensive LC-MS/MS mapping of the components of the SWI/SNF chromatin remodeling complex co-associated with CTCF including subunits belonging to the core, signature and ATPase modules. We further show that the localization patterns of representative SWI/SNF members significantly overlap with CTCF sites on transcriptionally active chromatin regions. Moreover, we provide evidence of a direct binding of the BRK-BRG1 domain to the zinc finger motifs 4-8 of CTCF, thus suggesting that these domains mediate the interaction of CTCF with the SWI/SNF complex. These findings provide an updated view of the cooperative nature between CTCF and the SWI/SNF ATP-dependent chromatin-remodeling complexes, an important step for understanding how these architectural proteins collaborate to shape the genome.
2021-09-09 | PXD022037 | Pride
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
Project description:Molecular mechanism of long-term memory has been extensively studied in the context of hippocampus-dependent recent memory examined within several days; however, months-old remote memory maintained in the cortex for long-term has not much been investigated at molecular levels yet. Various epigenetic mechanisms are known to be important for long-term memory, but how 3D chromatin architecture and its regulator molecules contribute to neuronal plasticity and memory consolidation are still largely unknown. To assess memory upon perturbation of 3D chromatin structure, we chose CCCTC-binding factor (CTCF), a seven-zinc finger protein well known for its role as a transcription factor and a chromatin regulator, and created the conditional knockout (cKO) mice, in which CTCF is lost in neurons during adulthood. Our CTCF cKO mice showed normal recent memory in contextual fear conditioning and spatial water maze task. However, they showed remarkable impairments in remote memory in both tasks. Underlying the remote memory-specific phenotypes, we found that loss of CTCF disrupts cortical long-term potentiation (LTP) but not hippocampal LTP. Through RNA-sequencing, we found that CTCF KD cultured cortical neurons have altered the expression of hundreds of genes, some of which we uncovered to be regulated by neuronal activity. These results suggest that remote memory storage in the cortex requires CTCF-mediated chromatin regulation in neurons while recent memory formation in the hippocampus does not.
2018-05-21 | GSE99230 | GEO
Project description:To identify genome-wide CCCTC binding factor (CTCF)-binding in A549 (ATCC CCL-185) and U2OS cells stably expressing rat GR (Rogatsky et al. , Mol Cell Biol, 1997. 17(6): p. 3181-93.) we performed ChIP-seq experiments upon hormone treatment (1.5 h, 1 M dexamethasone).
2018-04-12 | E-MTAB-5352 | biostudies-arrayexpress
Project description:Evolutionary comparison reveals that diverging CCCTC-binding factor (CTCF) sites are signatures of ancestral topological associating domains borders
| PRJNA278402 | ENA
Project description:The CCCTC-binding factor (CTCF) is a versatile transcriptional regulator required for embryogenesis, but its function in vascular development or in diseases with a vascular component is poorly understood. Here, we found that endothelial Ctcf is essential for mouse vascular development and limits accumulation of reactive oxygen species (ROS). Conditional knockout of Ctcf in endothelial progenitors and their descendants affected embryonic growth, and caused lethality at embryonic day 10.5 owing to defective yolk sac and placental vascular development. Analysis of global gene expression revealed Frataxin (Fxn), the gene mutated in Friedreich’s ataxia (FRDA), as the most strongly downregulated gene in Ctcfdeficient placental endothelial cells. Moreover, in vitro reporter assays showed that Ctcf activates the Fxn promoter in endothelial cells. Reactive oxygen species (ROS) are known to accumulate in the endothelium of FRDA patients. Importantly, Ctcf deficiency induced ROS-mediated DNA damage in endothelial cells in vitro, and in placental endothelium in vivo. Taken together, our findings indicate that, Ctcf promotes vascular development, and limits oxidative stress in endothelial cells, perhaps through activation of Fxn transcription. These results reveal a function for a Ctcf–Fxn transcriptional pathway in vascular development, and also suggest a potential mechanism for endothelial dysfunction in FRDA.
2018-02-23 | GSE109510 | GEO