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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Nucleosome dynamics specifies genome-wide binding of the male germ cell gene regulator CTCFL and of CTCF [MoGene-1_0 Expression]

ABSTRACT: CTCFL binding to DNA and the effect of CTCFL expression in ES cells RNA extracted from CTCFL induced and non-induced ES cells was hybridized on Affymetrix Mouse Gene 1.0ST arrays

ORGANISM(S): Mus musculus

SUBMITTER: frank sleutels

PROVIDER: E-GEOD-34092 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The male germ cell gene regulator CTCFL is functionally different from CTCF and binds CTCF-like consensus sites in a nucleosome composition-dependent manner.

Sleutels Frank F Soochit Widia W Bartkuhn Marek M Heath Helen H Dienstbach Sven S Bergmaier Philipp P Franke Vedran V Rosa-Garrido Manuel M van de Nobelen Suzanne S Caesar Lisa L van der Reijden Michael M Bryne Jan Christian JC van Ijcken Wilfred W Grootegoed J Anton JA Delgado M Dolores MD Lenhard Boris B Renkawitz Rainer R Grosveld Frank F Galjart Niels N

Epigenetics & chromatin 20120618 1

<h4>Background</h4>CTCF is a highly conserved and essential zinc finger protein expressed in virtually all cell types. In conjunction with cohesin, it organizes chromatin into loops, thereby regulating gene expression and epigenetic events. The function of CTCFL or BORIS, the testis-specific paralog of CTCF, is less clear.<h4>Results</h4>Using immunohistochemistry on testis sections and fluorescence-based microscopy on intact live seminiferous tubules, we show that CTCFL is only transiently pres ...[more]

PMID: 22709888

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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

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

Nucleosome dynamics specifies genome-wide binding of the male germ cell gene regulator CTCFL and of CTCF [MoGene-1_0 Expression]

Project description:CTCFL binding to DNA and the effect of CTCFL expression in ES cells

2012-07-25 | GSE34092 | GEO

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

2012-07-25 | GSE34094 | GEO

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [expression]

Project description:Scl/Tal1 confers hemogenic competence and prevents cardiomyogenesis in embryonic endothelium. Here we show that Scl both directly activates a broad gene regulatory network required for hematopoietic stem/progenitor cell (HS/PC) development, and represses transcriptional regulators required for cardiogenesis. Cardiac repression occurs during a short developmental window through Scl binding to distant cardiac enhancers that harbor H3K4me1 at this stage. Scl binding to hematopoietic regulators extends throughout HS/PC and erythroid development and spreads from distant enhancers to promoters. Surprisingly, Scl complex partners Gata 1 and 2 are dispensable for hematopoietic versus cardiac specification and Scl binding to the majority of its target genes. Nevertheless, Gata factors co-operate with Scl to activate selected transcription factors to facilitate HS/PC emergence from hemogenic endothelium. These results uncover a dual function for Scl in dictating hematopoietic versus cardiac fate choice and suggest a mechanism by which lineage-specific bHLH factors direct the divergence of competing fates. Examination of Scl target genes in ES cell derived day4 EB (embryoid body) Flk+ mesodermal cells

2015-01-01 | E-GEOD-47084 | biostudies-arrayexpress

Nucleosome dynamics specifies genome-wide binding of the male germ cell gene regulator CTCFL and of CTCF [Mouse430_2 Expression]

Project description:The effect of CTCFL mutation on the transcriptional program in testes Testis RNA extracted from CTCFL wildtype and mutant mice was hybridized on Affymetrix Mouse430_2 arrays

2012-07-24 | E-GEOD-34091 | biostudies-arrayexpress

Kdm2b facilitates iPS (induced pluripotent stem cells) cell generation

Project description:RNA samples were extracted from mouse embryonic fibroblast transduced with Oct4, Sox2 and Klf4 (OSK) or OSK plus Kdm2b at post-transduction day 4, 8 and 12.

2012-04-22 | E-MEXP-3433 | biostudies-arrayexpress

Cdx2 Binding Sites On Cdx2 Expressing ES Cells

Project description:A) Chromatins were prepared from Cdx2-inducible ES cells cultured for 48 - 60 hours in the Dox+ and Dox- conditions. Chromatin immunoprecipitation (ChIP) was carried out by using anti-FLAG M2 affinity gel. ChIP product was tested by Western blotting using anti-FLAG antibody. Nuclear extract from ES cells cultured for 48 - 60 hours in Dox+ and Dox- condition was used for the Western blot. B) CDX2 ChIP-Seq peaks in the Hoxa7 gene region. UCSC Mouse Mm9 browser view of Hoxa7 gene locus after mapping CDX2 ChIP-Seq tags locations in the wiggle format. CDX2 ChIP-Seq peaks are shown in red color. C) Cdx2 ChIP-Seq result was verified by qPCR. Target genes were indicated in (G). Primers flanking a promoter region of Hbb-b1 and Pou5f1 as well as a gene desert region in chromosome 3 were used as negative controls. Primers flanking of Actb gene promoter were used for normalization. The relative enrichment of CDX2 binding was indicated as fold change. (D) CDX2-binding motifs identified with CisFinder using 200 bp sequences centered at ChIP sites. (F) Potential CDX2-direct target genes based on ChIP-Seq and the alteration of expression by Cdx2-overexpression. (G) Identification of CDX2 target genes by combining information on binding sites with gene expression response to Cdx2 over-expression Chromatin IP against CDX2-Flag fusion protein. MC1 ES cells were genetically modified for ROSA26 locus to have Tet-Off expression cassette for C-terminal FLAG tagged Cdx2. The peaks are obtained from the Eland Multi Alignment file. The number of tags in peaks was compared with the number of tags in the control sample for the same region corrected by the total coverage of tags. See supplemental file of the paper for details.

2009-10-01 | E-GEOD-14586 | 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

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [RNA-seq]

Project description:Scl/Tal1 confers hemogenic competence and prevents cardiomyogenesis in embryonic endothelium. Here we show that Scl both directly activates a broad gene regulatory network required for hematopoietic stem/progenitor cell (HS/PC) development, and represses transcriptional regulators required for cardiogenesis. Cardiac repression occurs during a short developmental window through Scl binding to distant cardiac enhancers that harbor H3K4me1 at this stage. Scl binding to hematopoietic regulators extends throughout HS/PC and erythroid development and spreads from distant enhancers to promoters. Surprisingly, Scl complex partners Gata 1 and 2 are dispensable for hematopoietic versus cardiac specification and Scl binding to the majority of its target genes. Nevertheless, Gata factors co-operate with Scl to activate selected transcription factors to facilitate HS/PC emergence from hemogenic endothelium. These results uncover a dual function for Scl in dictating hematopoietic versus cardiac fate choice and suggest a mechanism by which lineage-specific bHLH factors direct the divergence of competing fates. Examination of Scl and Gata 1 & 2 target genes in ES cell derived day4.75 EB (embryoid body) Tie2+CD31+CD41- endothelial cells

2015-01-01 | E-GEOD-47083 | biostudies-arrayexpress

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