Disentangling the architectural and non-architectural functions of CTCF and cohesin in global gene regulation [ChIP-Seq]
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PROVIDER: PRJNA1092103 | ENA |
REPOSITORIES: ENA
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Project description:Disentangling the architectural and non-architectural functions of CTCF and cohesin in global gene regulation
| PRJNA1092101 | ENA
Project description:Disentangling the architectural and non-architectural functions of CTCF and cohesin in global gene regulation [EU-Seq]
| PRJNA1092105 | ENA
Project description:Disentangling the architectural and non-architectural functions of CTCF and cohesin in global gene regulation [ATAC-Seq]
| PRJNA1092104 | ENA
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
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 | GSE262520 | GEO
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 | GSE262519 | GEO
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 | GSE262516 | GEO
Project description:Eukaryotic genomes are assembled into chromatin by histones and extruded into loops by cohesin. These mechanisms control important genomic functions, but whether histones and cohesin cooperate in genome regulation is poorly understood. Here we identify Phf2, a member of the Jumonji-C family of histone demethylases, as a cohesin-interacting protein. Phf2 binds to H3K4me3 nucleosomes at active transcription start sites (TSSs) but also co-localizes with cohesin. Cohesin depletion reduces Phf2 binding at sites lacking H3K4me3, and depletion of Wapl and CTCF re-positions Phf2 together with cohesin in the genome, resulting in the accumulation of both proteins in vermicelli and cohesin islands. Conversely, Phf2 depletion reduces cohesin binding at TSSs lacking CTCF, decreases the number of short cohesin loops, but increases the length of heterochromatic B compartments. These results suggest that Phf2 is an ‘epigenetic reader’, which is translocated through the genome by cohesin-mediated DNA loop extrusion, and which recruits cohesin to active TSSs and limits the size of B compartments. These findings reveal an unexpected degree of cooperativity between epigenetic and architectural mechanisms of eukaryotic genome regulation.
2024-12-18 | PXD057926 | Pride
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:Chromosome conformation capture approaches have shown that interphase chromatin is organized into an architectural framework of Mb-sized compartments and sub-Mb-sized topological domains. Cohesin controls chromosome topology to facilitate DNA repair and chromosome segregation in cycling cells, and also associates with active enhancers and promoters and with CTCF to form long-range interactions important for gene regulation. We find that architectural compartments - a major feature of interphase chromatin organization – are maintained in non-cycling mouse thymocytes after genetic depletion of cohesin in vivo. Cohesin was however required for specific long-range interactions within permissive (A-type) compartments, where cohesin-regulated genes reside. Cohesin depletion diminished interactions between cohesin-bound sites, while alternative interactions between chromatin features associated with transcriptional activation and repression became more prominent, with corresponding changes in gene expression. Our findings indicate that cohesin-mediated long-range interactions facilitate discrete gene expression states within pre-existing chromosomal compartments.
2013-08-13 | GSE48763 | GEO