The CTCF paralog CTCFL disrupts cohesin at active promoters.
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ABSTRACT:
PROVIDER: PRJNA278933 | ENA |
REPOSITORIES: ENA
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Project description:The CTCF paralog CTCFL disrupts cohesin at active promoters. [mouse]
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Project description:The CTCF paralog CTCFL disrupts cohesin at active promoters. [human]
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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: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:Ctcfl, a paralog of Ctcf, also known as BORIS (Brother of Regulator of Imprinted Sites), is a testis expressed gene whose function is largely unknown. As a cancer testis antigen, it is often expressed in tumor cells and also seen in two benign human vascular malformations, juvenile angiofibromas (JA) and infantile hemangiomas (IH). To better understand the function of Ctcfl we created tetracycline-inducible Ctcfl transgenic mice. We show that when Ctcfl expression is induced during embryogenesis, it results in intrauterine growth retardation, developmental eye malformations, multi-organ pathologies, vascular defects, and early neonatal lethality. This phenotype resembles prior mouse models which perturb the TGFB pathway. Embryonic stem cells with the Ctcfl transgene reproduce the same phenotype in ES cell: tetraploid chimeras. RNA-Seq of the Ctcfl ES cells revealed 14 genes, including a number of transcription factors/ co-activators, and signal transduction pathway genes that are significantly deregulated by Ctcfl expression. Bioinformatics analysis revealed the TGFB pathway to be most affected by embryonic Ctcfl expression. We propose that our transgenic mice reiterate a developmental program normally reserved for spermatogenesis that results in multiple organ pathology when expressed in embryogenesis as a result of the TGFB pathway dysregulation. Understanding of the phenotypic consequence of Ctcfl expression in non-testicular cells and elucidating downstream targets of Ctcfl has the potential to explain its role as a cancer testis antigen (CTA) and its involvement in two, if not more, human vascular malformations.
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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.
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