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Low affinity CTCF binding drives transcriptional regulation whereas high affinity binding encompasses architectural functions.

ABSTRACT: Low affinity CTCF binding drives transcriptional regulation whereas high affinity binding encompasses architectural functions.

PROVIDER: PRJNA856492 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20016460.fastq.gz	Fastqsanger.gz
	SRR20016461.fastq.gz	Fastqsanger.gz
	SRR20016462.fastq.gz	Fastqsanger.gz
	SRR20016463.fastq.gz	Fastqsanger.gz
	SRR20016464.fastq.gz	Fastqsanger.gz

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Low affinity CTCF binding drives transcriptional regulation whereas high affinity binding encompasses architectural functions.

Project description:This SuperSeries is composed of the SubSeries listed below. CTCF is a DNA-binding protein which plays critical roles in chromatin structure organization and transcriptional regulation; however, little is known about the functional determinants of different CTCF binding sites (CBS). Using a conditional mouse model, we have identified one set of CBSs that are lost upon CTCF depletion (lost CBSs) and another set that persists (retained CBSs). Retained CBSs are more similar to the consensus CTCF binding sequence and usually span tandem CTCF peaks. Lost CBSs are enriched at enhancers and promoters and associate with active chromatin marks and higher transcriptional activity. In contrast, retained CBSs are enriched at TAD and loop boundaries. Integration of ChIP-seq and RNA-seq data has revealed that retained CBSs are located at the boundaries between distinct chromatin states, acting as chromatin barriers. Our results provide evidence that transient, lost CBSs are involved in transcriptional regulation, whereas retained CBSs are critical for establishing higher-order chromatin architecture.

2023-02-10 | GSE207640 | GEO

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

Deciphering the role of RNA in regulating CTCF’s DNA binding affinity in leukemia cells [CTCF-ChIP]

Project description:CTCF, a highly studied transcription factor, is essential for chromatin interaction maintenance. Several independent studies have reported that CTCF interacts with RNAs in vitro and in cells. Yet continuous debates about the authenticity of the RNA-binding affinity of CTCF and its biological role remain in large part due to limited research techniques available, such as CLIP-seq. Here, we investigated the role RNA plays on CTCF’s transcription factor function through its chromatin occupancy. To systematically investigate whether RNAs affect CTCF’s ability to bind DNA, we perturbed CTCF-RNA interactions by three independent approaches and examined CTCF genome occupancy by ChIP-seq. Although RnaseA A and Triptolide treatment each affected a certain number of CTCF-binding peaks, few peaks overlapped between treatment groups indicating the effect of RNA in regulating CTCF’s DNA binding affinity was modest and variable between loci. In addition, limited transcriptional or chromatin accessibility changes were observed between cells expressing wild-type CTCF or CTCF lacking the RNA binding region. Our data provide a complementary approach and in silico evidence to reconsider the significance of RNA affecting CTCF’s DNA-binding affinity in a global manner.

2024-11-11 | GSE281633 | GEO

Deciphering the role of RNA in regulating CTCF’s DNA binding affinity in leukemia cells [CTCF-HA-ChIP]

Project description:CTCF is the most studied transcription factor, which is essential for chromatin interaction maintenance. Although several independent studies reported that CTCF protein could pull down RNAs in vitro and in cells, there are continuous debates about authenticity of the RNA-binding affinity of CTCF and its biological role, mainly due to the concerns of limited research techniques such as CLIP-seq. To systematically investigate the RNA-interaction with CTCF and the impact on gene regulation, we conducted in vivo CTCF ChIP-seq under three conditions, including RNase A treatment, Triptolide-mediated transcription inhibition and auxin-inducible degron mediated RNA-binding domain mutant swap. Our results consistently suggest that when RNA-interaction with CTCF protein was impaired in vivo, the DNA occupancy of CTCF remains the same at the genome-wide scale. Our data provide a complementary approach and in silico evidence to re-considerate the role of RNA-binding affinity of CTCF.

2024-03-08 | GSE261176 | GEO

Exploring the interaction between the SWI/SNF chromatin remodeling complex and the zinc finger factor CTCF

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

Advanced auxin-inducible degron system deciphers unique functions of CTCF in transcriptional regulation [ChIP-seq]

Project description:ChIPseq was performed on cells depleted for CTCF by AID2 auxin degradation to examine CTCF DNA binding affinity. ChIP seq was also performed on cells depleted for endogenous CTCF and expressing HA tagged WT CTCF and CTCF mutants (deltaZF1, deltaZF10 and deltaRBR) to examine how functional deletions affect CTCF DNA binding affinity.

2022-12-28 | GSE205408 | GEO

BRD2 cooperates with CTCF to enforce transcriptional and architectural boundaries

Project description:BET (bromodomain and extraterminal motif) proteins are pharmacologic targets for the treatment of diverse diseases, yet the roles of individual BET family members remain unclear. We find that BRD2 colocalizes with the architectural/insulator protein CCCTC-binding factor (CTCF) genome-wide. To test a role for BRD2 in chromatin architecture we performed HiC in uninduced G1E-ER4 cells (-GATA1), and compared it to HiC in BRD2-depleted G1E-ER4 cells

2017-03-31 | GSE95476 | GEO

CTCF binding polarity determines chromatin looping [4C]

2015-10-29 | GSE72539 | GEO

Distinct properties and functions of CTCF revealed by a rapidly inducible degron system [PRO-Seq]

Project description:We coupled an auxin-induced degron (AID) system with precision nuclear run-on (PRO-seq). Oriented CTCF motifs in gene bodies are associated with transcriptional stalling in a manner ostensibly independent of bound CTCF. CTCF binding sites display highly variable resistance to degradation, with persistent sites displaying architectural related features.

2021-02-23 | GSE150414 | GEO

Distinct properties and functions of CTCF revealed by a rapidly inducible degron system [ChIP-Seq]

2021-02-23 | GSE150415 | GEO