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Nucleosome dynamics specifies genome-wide binding of the male germ cell gene regulator CTCFL and of CTCF [ChIP-Seq]

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE34094 | GEO | 2012/07/25

SECONDARY ACCESSION(S): PRJNA156497

REPOSITORIES: GEO

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Nucleosome dynamics specifies genome-wide binding of the male germ cell gene regulator CTCFL and of CTCF [ChIP-Seq]

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

BORIS/CTCFL epigenetically reprograms clustered CTCF binding sites into alternative transcriptional start sites.

Project description:Pervasive usage of alternative promoters leads to deregulation of gene expression in carcinogenesis and may drive the emergence of new genes in spermatogenesis. However, little is known regarding the mechanisms underpinning the activation of alternative promoters. In our present study, we uncovered a novel mechanism by which alternative cancer-testis-specific transcription is activated from the intergenic and intronic clustered CTCF binding sites, which are transcriptionally inert in normal somatic cells. BORIS/CTCFL, a paralog of CTCF with cancer-testis-specific expression forms a heterodimer with CTCF at the clustered binding sites thus triggering epigenetic reprogramming of these sites into units of active transcription. BORIS binding to CTCF sites leads to the recruitment of chromatin-remodeling factor SRCAP, with subsequent replacement of H2A histone with H2A.Z, therefore creating a more relaxed chromatin state in the nucleosomes flanking the clustered binding sites. This facilitates opening of chromatin beyond CTCF/BORIS binding sites and paves the way to the recruitment of multiple additional transcription factors, thereby activating transcription from a given binding site. We demonstrate that the CTCF binding sites, epigenetically reprogrammed by ectopic BORIS expression can drive the expression of cancer-testis genes, long-noncoding RNAs, retro-pseudogenes, and dormant transposable elements harbored by activated long transcripts. Taking together, our results reveal that BORIS functions as a transcription factor that epigenetically reprograms clustered CTCF binding sites into transcriptional start sites, promoting transcription from alternative promoters in both germ cells and cancer cells.

2024-01-03 | GSE207058 | GEO

Human tandem repeat custom custom microarray ChIP-chip with anti-CTCF and anti-CTCFL/BORIS antibodies in K562 cell line

Project description:A common aberration in cancer is the activation of germline-specific proteins. The DNA-binding proteins among them generate novel chromatin states, not found in normal cells. The chromatin architecture protein CTCF has a germline-specific paralog BORIS/CTCFL, which is often erroneously activated in cancers. Another common feature of malignancies is the changed expression and epigenetic states of genomic repeats. The investigation of BORIS and CTCF binding to DNA repeats in cancer cell lines by ChIP-chip revealed three classes: elements cohabited by BORIS and CTCF, CTCF-bound only, or BORIS-only.

2016-08-17 | GSE84326 | GEO

Gene expression changes after Ctcfl overexpression in NIH3T3 cells.

Project description:The two paralogous zinc finger factors CTCF and CTCFL differ in expression such that CTCF is ubiquitously expressed, whereas CTCFL is found during spermatogenesis and in some cancer types. Both factors share the highly conserved DNA binding domain and are bound to DNA sequences with an identical consensus. Here we analyzed the differential gene expression effect mediated by expression of Ctcfl in undifferentiated and differentiated NIH3T3 cell.

2018-05-30 | GSE103196 | GEO

Gene expression changes after Ctcfl overexpression in undifferentiated and differentiated p19 cells.

2018-05-30 | GSE103197 | GEO

Nucleosome dynamics specifies genome-wide binding of the male germ cell gene regulator CTCFL and of CTCF

Project description:This SuperSeries is composed of the following subset Series: GSE34091: Nucleosome dynamics specifies genome-wide binding of the male germ cell gene regulator CTCFL and of CTCF [Mouse430_2 Expression] GSE34092: Nucleosome dynamics specifies genome-wide binding of the male germ cell gene regulator CTCFL and of CTCF [MoGene-1_0 Expression] GSE34094: Nucleosome dynamics specifies genome-wide binding of the male germ cell gene regulator CTCFL and of CTCF [ChIP-Seq] Refer to individual Series

2012-07-24 | E-GEOD-34093 | biostudies-arrayexpress

Comparative analyses of CTCF and BORIS occupancies uncover two distinct classes of CTCF binding genomic regions

Project description:CTCF and BORIS (CTCFL), two paralogous mammalian proteins sharing nearly identical DNA binding domains, are thought to function in mutually exclusive manners in DNA binding and transcriptional regulation. Here we show that these two proteins co-occupy a specific subset of regulatory elements consisting of clustered CTCF binding motifs (termed 2xCTSes). BORIS occupancy at 2xCTSes is largely invariant in BORIS-positive cancer cells, with the genomic pattern recapitulating the germline-specific BORIS binding to chromatin. In contrast to the single-motif CTCF target sites (1xCTSes), the 2xCTS elements are preferentially found at active promoters and enhancers, both in cancer and germ cells. 2xCTSes are also enriched in genomic regions that escape histone to protamine replacement in human and mouse sperm. Depletion of BORIS gene leads to altered transcription of a large number of genes and the differentiation of K562 cells, while the ectopic expression of this CTCF paralog leads to specific changes in transcription in MCF7 cells. In summary, we discover two functionally and structurally different classes of CTCF binding regions, 2xCTSes and 1xCTSes, revealed by their predisposition to bind BORIS. We propose that 2xCTSes play key roles in the transcriptional program of cancer and germ cells Genome-wide mapping of CTCF and BORIS occupancies in both germ and cancer cells. ChIP-seq and expression profiling by high throughput sequencing

2015-07-23 | E-GEOD-70764 | biostudies-arrayexpress

RNA-Seq of Ctcfl transgenic mouse ES cells

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.

2015-08-19 | GSE72178 | GEO

BORIS/CTCFL epigenetically reprograms clustered CTCF binding sites into alternative transcriptional start sites.

Project description:BORIS/CTCFL epigenetically reprograms clustered CTCF binding sites into alternative transcriptional start sites.

| PRJNA853953 | ENA

RNA-seq analysis of BORIS/CTCFL knockdown in K562 cell line

Project description:The study involved transcriptome analysis using RNA-seq knockdown of BORIS/CTCFL gene expression in K652 cancer cell line using inducible shRNA. The K562 cell line is the only cancer cell line that is known to be dependent on BORIS for proliferation and self-renewal of stemness. The goal of the study was to investigate the early/immediate transcriptional response to BORIS downregulation (over 10-fold reduction in protein level) using an inducible shRNA.

2017-09-25 | GSE99825 | GEO

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