Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA278936 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The CTCF paralog CTCFL disrupts cohesin at active promoters.
| PRJNA278933 | ENA
Project description:The CTCF paralog CTCFL disrupts cohesin at active promoters. [human]
| PRJNA278937 | ENA
Project description:CTCF and CTCFL DNA binding profile in CTCFL induced and non-induced ES cells.CTCF is a highly conserved and essential zinc finger protein that in conjunction with cohesin organizes chromatin into loops, thereby regulating gene expression and epigenetic events. The function of CTCFL or BORIS, the testis-specific paralogue of CTCF, is less clear. Here, we show that CTCFL is only transiently present during spermatogenesis, prior to the onset of meiosis, when the protein co-localizes in nuclei with ubiquitously expressed CTCF. Our data show that CTCFL is functionally different from CTCF and its absence in mice causes sub-fertility due to a partially penetrant testicular atrophy. Genome-wide studies reveal that CTCFL and CTCF bind similar consensus sequences. However, only ~2000 out of the ~5,700 CTCFL and ~31,000 CTCF binding sites overlap. CTCFL binds promoters with loosely assembled nucleosomes, whereas CTCF favors consensus sites surrounded by phased nucleosomes. Thus, nucleosome dynamics specifies the genome-wide binding of CTCFL and CTCF. We propose that the transient expression of CTCFL in spermatogonia and preleptotene spermatocytes serves to occupy a subset of promoters and maintain the expression of male germ cell genes ChIP-seq for CTCF (with CTCF antibody) and CTCFL (with V5 antibody) in CTCFL_V5_GFP induced and non-induced ES cells
2012-07-25 | E-GEOD-34094 | biostudies-arrayexpress
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:CTCF and CTCFL DNA binding profile in CTCFL induced and non-induced ES cells.CTCF is a highly conserved and essential zinc finger protein that in conjunction with cohesin organizes chromatin into loops, thereby regulating gene expression and epigenetic events. The function of CTCFL or BORIS, the testis-specific paralogue of CTCF, is less clear. Here, we show that CTCFL is only transiently present during spermatogenesis, prior to the onset of meiosis, when the protein co-localizes in nuclei with ubiquitously expressed CTCF. Our data show that CTCFL is functionally different from CTCF and its absence in mice causes sub-fertility due to a partially penetrant testicular atrophy. Genome-wide studies reveal that CTCFL and CTCF bind similar consensus sequences. However, only ~2000 out of the ~5,700 CTCFL and ~31,000 CTCF binding sites overlap. CTCFL binds promoters with loosely assembled nucleosomes, whereas CTCF favors consensus sites surrounded by phased nucleosomes. Thus, nucleosome dynamics specifies the genome-wide binding of CTCFL and CTCF. We propose that the transient expression of CTCFL in spermatogonia and preleptotene spermatocytes serves to occupy a subset of promoters and maintain the expression of male germ cell genes
2012-07-25 | GSE34094 | GEO
Project description:The DNA-binding protein CTCF and the cohesin complex function together to shape chromatin architecture in mammalian cells, but the molecular details of this process remain unclear. We demonstrate that a 79 amino acid region within the CTCF N-terminal domain but not the C-terminus is necessary for cohesin positioning at CTCF binding sites and chromatin loop formation. However, the N-terminus of CTCF, when fused to artificial zinc fingers that do not bind to CTCF DNA binding sites was not sufficient to redirect cohesin to different genomic locations, indicating that cohesin positioning by CTCF does not involve direct protein-protein interactions with cohesin subunits. BORIS (CTCFL), a germline-specific paralog of CTCF was unable to anchor cohesin to CTCF DNA binding sites. Furthermore, CTCF-BORIS Chimeric constructs provided evidence that both the first two CTCF zinc fingers and, likely, the 3D geometry of CTCF-DNA complexes are involved in cohesin retention. Moreover, we were able to convert BORIS into CTCF with respect to cohesin positioning, thus providing additional molecular details of the cohesin retention function of CTCF. Our data suggest that the N-terminus of CTCF and the 3D spatial conformation of the CTCF-DNA complex act as a roadblock to constrain cohesin movement along DNA.
2020-01-01 | GSE136122 | GEO
Project description:The DNA-binding protein CTCF and the cohesin complex function together to shape chromatin architecture in mammalian cells, but the molecular details of this process remain unclear. We demonstrate that a 79 amino acid region within the CTCF N-terminal domain but not the C-terminus is necessary for cohesin positioning at CTCF binding sites and chromatin loop formation. However, the N-terminus of CTCF, when fused to artificial zinc fingers that do not bind to CTCF DNA binding sites was not sufficient to redirect cohesin to different genomic locations, indicating that cohesin positioning by CTCF does not involve direct protein-protein interactions with cohesin subunits. BORIS (CTCFL), a germlinespecific paralog of CTCF was unable to anchor cohesin to CTCF DNA binding sites. Furthermore, CTCF-BORIS Chimeric constructs provided evidence that both the first two CTCF zinc fingers and, likely, the 3D geometry of CTCF-DNA complexes are involved in cohesin retention. Moreover, we were able to convert BORIS into CTCF with respect to cohesin positioning, thus providing additional molecular details of the cohesin retention function of CTCF. Our data suggest that the N-terminus of CTCF and the 3D spatial conformation of the CTCF-DNA complex act as a roadblock to constrain cohesin movement along DNA.
2020-01-01 | GSE137216 | GEO