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Disentangling the architectural and non-architectural functions of CTCF and cohesin in global gene regulation [ChIP-Seq]

ABSTRACT: Cohesin- and CTCF-mediated chromatin loops shape enhancer-promoter interactions, but their global impact on gene regulation remains unclear. We show that cohesin and CTCF regulate hundreds of genes in mouse cells, though the magnitude of expression changes is modest. Acute loss of cohesin loops mainly downregulates CBP/p300-dependent enhancer targets, while CTCF depletion can both up- and downregulate putative enhancer targets. Interestingly, beyond regulating enhancer-dependent transcription via loop anchoring, CTCF acts as a transcriptional activator or repressor of sense and antisense transcripts, depending on its binding position and orientation in promoters. Mechanistically, promoter-bound CTCF enhances DNA accessibility and RNA polymerase II recruitment, thereby activating housekeeping genes essential for mammalian cell proliferation. CTCF’s transcriptional activation function—but not its loop-anchoring role—is shared with its vertebrate-specific paralog, CTCFL. These findings resolve cohesin and CTCF’s roles in global gene regulation, offering a unified model that integrates their enhancer-dependent and -independent functions in transcription control.

ORGANISM(S): Mus musculus

PROVIDER: GSE262519 | GEO | 2025/08/27

REPOSITORIES: GEO

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Disentangling the architectural and non-architectural functions of CTCF and cohesin in global gene regulation

Project description:Cohesin- and CTCF-mediated chromatin loops shape enhancer-promoter interactions, but their global impact on gene regulation remains unclear. We show that cohesin and CTCF regulate hundreds of genes in mouse cells, though the magnitude of expression changes is modest. Acute loss of cohesin loops mainly downregulates CBP/p300-dependent enhancer targets, while CTCF depletion can both up- and downregulate putative enhancer targets. Interestingly, beyond regulating enhancer-dependent transcription via loop anchoring, CTCF acts as a transcriptional activator or repressor of sense and antisense transcripts, depending on its binding position and orientation in promoters. Mechanistically, promoter-bound CTCF enhances DNA accessibility and RNA polymerase II recruitment, thereby activating housekeeping genes essential for mammalian cell proliferation. CTCF’s transcriptional activation function—but not its loop-anchoring role—is shared with its vertebrate-specific paralog, CTCFL. These findings resolve cohesin and CTCF’s roles in global gene regulation, offering a unified model that integrates their enhancer-dependent and -independent functions in transcription control.

2025-08-27 | GSE262521 | GEO

Disentangling the architectural and non-architectural functions of CTCF and cohesin in global gene regulation [EU-Seq]

2025-08-27 | GSE262520 | GEO

Disentangling the architectural and non-architectural functions of CTCF and cohesin in global gene regulation [ATAC-Seq]

2025-08-27 | GSE262516 | GEO

Computational prediction of CTCF/cohesin-based intra-TAD (sbTAD) loops that insulate chromatin contacts and gene expression in mouse liver

Project description:This SuperSeries is composed of the SubSeries listed below, and presents the high throuput sequencing datasets that were generated as part of a larger study that investigates the role of CTCF and cohesin as key drivers of 3D-nuclear organization, anchoring the megabase-scale Topologically Associating Domains (TADs) that segment the genome. This study presents and validates a computational method to predict cohesin-and-CTCF binding sites that form intra-TAD DNA loops. The intra-TAD loop anchors identified are structurally indistinguishable from TAD anchors regarding binding partners, sequence conservation, and resistance to cohesin knockdown; further, the intra-TAD loops retain key functional features of TADs, including chromatin contact insulation, blockage of repressive histone mark spread, and ubiquity across tissues. The intra-TAD loops are proposed to be formed by the same loop extrusion mechanism as the larger TAD loops; their shorter length enables finer regulatory control in restricting enhancer-promoter interactions, which enables selective, high-level expression of gene targets of super-enhancers and genes located within repressive nuclear compartments. These findings elucidate the role of intra-TAD cohesin-and-CTCF binding in nuclear organization associated with widespread insulation of distal enhancer activity.

2018-05-11 | GSE102999 | GEO

CCCTC-binding Factor N-terminal Domain Regulates Clustered Protocadherin Gene Expression by Enhancing Cohesin Processivity [4C-Seq]

Project description:CTCF (CCCTC-binding factor) instructs 3D genome folding by anchoring or forestalling cohesin loop extrusion, but the exact mechanism remains obscure. Here, using clustered protocadherins (cPcdh) as model genes, we report that CTCF assists or facilitates cohesin loop extrusion by enhancing its processivity. Specifically, we show that, compared with the Pcdh alpha and gamma clusters, the Pcdh beta cluster is greatly affected upon CTCF Y226A/F228A mutation in the N-terminal domain. Given the long-range distance of the Pcdh beta cluster from the distal enhancer, this finding has interesting implications in CTCF regulation of cohesin processivity along the linear chromatin during DNA loop extrusion. In particular, the effect on cohesin processivity upon CTCF Y226A/F228A mutation is conspicuously similar to that of WAPL overexpression, suggesting that, in addition to the general view of blocking or forestalling cohesin, CTCF may also enhances or facilitates cohesin loop extrusion.

2025-02-15 | GSE285579 | GEO

CCCTC-binding Factor N-terminal Domain Regulates Clustered Protocadherin Gene Expression by Enhancing Cohesin Processivity [RNA-Seq]

2025-02-15 | GSE285577 | GEO

CCCTC-binding Factor N-terminal Domain Regulates Clustered Protocadherin Gene Expression by Enhancing Cohesin Processivity

2025-02-15 | GSE287859 | GEO

CTCF N-terminal Domain Regulates Clustered Protocadherin Gene Expression by Enhancing Cohesin Processivity [ChIP-seq]

Project description:CTCF structures 3D genome folding by anchoring or forestalling cohesin loop extrusion, but the exact mechanism remains obscure. Here, using clustered protocadherins (cPcdh) as model genes, we report that CTCF stabilizes or facilitates cohesin loop extrusion by enhancing its processivity. Specifically, we show that, compared with the Pcdh alpha and gamma clusters, the Pcdh beta cluster is greatly affected upon CTCFY226A/F228A mutation in the N-terminal domain. Given the long-range distance of the Pcdh beta cluster from the distal enhancer, this finding has interesting implications in CTCF regulation of cohesin processivity along the linear chromatin during DNA loop extrusion. In particular, the effect on cohesin processivity upon CTCFY226A/F228A mutation is conspicuously similar to that of WAPL overexpression, demonstrating that, contrary to the general view of blocking or forestalling cohesin, CTCF actually enhances or facilitates cohesin loop extrusion.

2025-02-15 | GSE285578 | GEO

3D regulatory landscape of human naive pluripotency [ChIP-Seq]

Project description:The control of cell identity is orchestrated by transcriptional and chromatin regulators in the context of specific chromosome structures. With the recent isolation of human naive embryonic stem cells (ESCs) representative of the ground state of pluripotency, it is possible to deduce this regulatory landscape in one of the earliest stages of human development. Here we generate cohesin ChIA-PET chromatin interaction data in naive and primed human ESCs and use it to reconstruct and compare the 3D regulatory landscapes of these two stages of early human development. The results reveal shared and stage-specific regulatory landscapes of topological domains and their subdomains, which consist of CTCF-CTCF/cohesin loops and enhancer-promoter/cohesin loops. The enhancer-promoter loop data reveal that genes with key roles in pluripotency are nearly always regulated by one or more super-enhancers, and show that these genes tend to occur in insulated neighborhoods. Our results reveal the key features of the 3D regulatory landscape of early human cells that form the foundation for embryonic development. ChIP-seq data from naive and primed human embroynic stem cells.

2015-11-22 | E-GEOD-69646 | biostudies-arrayexpress

3D regulatory landscape of human naive pluripotency [RNA-Seq]

Project description:The control of cell identity is orchestrated by transcriptional and chromatin regulators in the context of specific chromosome structures. With the recent isolation of human naive embryonic stem cells (ESCs) representative of the ground state of pluripotency, it is possible to deduce this regulatory landscape in one of the earliest stages of human development. Here we generate cohesin ChIA-PET chromatin interaction data in naive and primed human ESCs and use it to reconstruct and compare the 3D regulatory landscapes of these two stages of early human development. The results reveal shared and stage-specific regulatory landscapes of topological domains and their subdomains, which consist of CTCF-CTCF/cohesin loops and enhancer-promoter/cohesin loops. The enhancer-promoter loop data reveal that genes with key roles in pluripotency are nearly always regulated by one or more super-enhancers, and show that these genes tend to occur in insulated neighborhoods. Our results reveal the key features of the 3D regulatory landscape of early human cells that form the foundation for embryonic development. Polyadenylated RNA-seq from naive and primed human embroynic stem cells.

2015-11-22 | E-GEOD-69692 | biostudies-arrayexpress

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