CTCF binding patterns in mouse trophoblast stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE40667 | GEO | 2012/09/08
SECONDARY ACCESSION(S): PRJNA174628
REPOSITORIES: GEO
Similar Datasets
Project description:This Series reports data from a CTCF ChIP-Seq experiment performed in F1-hybrid mouse trophoblast stem cells (TSCs). The data are part of a larger study examining inactive X gene expression and chromatin states, reported as GEO Series GSE39406. Included for this dataset are FASTQ files, BED alignments and WIG files with coordinates relative to UCSC genome build mm9, and _snp files that report the location of all SNP-overlapping reads Single CTCF ChIP-Seq experiment
2012-09-08 | E-GEOD-40667 | biostudies-arrayexpress
Project description:The inactive X chromosome’s (Xi) physical territory is microscopically devoid of transcriptional hallmarks and enriched in silencing-associated modifications. How these microscopic signatures relate to specific Xi sequence is unknown. This study reports the profiling of Xi gene expression and chromatin states at high-resolution via allele-specific sequencing in F1 hybrid mouse trophoblast stem cells (TSCs). Datasets provided include those generated from strand-specific RNA-Seq, ChIP-Seq, FAIRE-Seq, and DNase-Seq protocols. Included for each dataset are FASTQ files, BED alignments and WIG files with coordinates relative to UCSC genome build mm9, and _snp files that report the location of all SNP-overlapping reads.
2012-11-21 | GSE39406 | GEO
Project description:The inactive X chromosome’s (Xi) physical territory is microscopically devoid of transcriptional hallmarks and enriched in silencing-associated modifications. How these microscopic signatures relate to specific Xi sequence is unknown. This study reports the profiling of Xi gene expression and chromatin states at high-resolution via allele-specific sequencing in F1 hybrid mouse trophoblast stem cells (TSCs). Datasets provided include those generated from strand-specific RNA-Seq, ChIP-Seq, FAIRE-Seq, and DNase-Seq protocols. Included for each dataset are FASTQ files, BED alignments and WIG files with coordinates relative to UCSC genome build mm9, and _snp files that report the location of all SNP-overlapping reads. The F1 TSC lines profiled were generated from crosses between CAST/EiJ (Cast) and C57BL/6J (B6) mice. C/B denotes a Cast mother and B6 father, and B/C denotes a B6 mother and Cast father.
2012-11-21 | E-GEOD-39406 | biostudies-arrayexpress
Project description:The spatial proximity between regulatory elements and their target genes has a profound affect on gene expression. X Chromosome Inactivation (XCI) is an epigenetic process by which an entire chromosome is rendered, for the most part, transcriptionally silent. A few genes are known to escape XCI and the mechanism for this escape remains unclear. Here, using mouse trophectodermal stem cells, we address whether specific chromosomal interactions facilitate escape from XCI by bringing escape-specific regulatory elements in close proximity to gene promoters. Our results suggest a model where escape from XCI occurs within topologically associated domains. As such, escaping genes and the regulatory sequences required for their escape are likely located within close linear proximity to each other. The datasets provided include those generated from allele-specific 4C-Seq of genes escaping XCI, genes subject to XCI, and non-genic regions of the X chromosome. FASTQ files, text files containing genomic coordiantes, and BED aligmnets are provided. All sequences were mapped relative to mouse genome build mm9.
2014-03-26 | GSE49111 | GEO
Project description:Stem cells reside in specific niches providing stemness-maintaining environments. Thus, the regulated migration from these niches is associated with differentiation onset. However, mechanisms retaining stem cells in their niche remain poorly understood. Here, we show that the epigenetic regulator lysine-specific demethylase 1 (Lsd1) organises the trophoblast niche of the early mouse embryo by coordinating migration and invasion of trophoblast stem cells (TSCs). Lsd1 deficiency leads to the depletion of the stem cell pool resulting from precocious migration of TSCs. Migration is induced by premature expression of the transcription factor Ovol2 that is repressed by Lsd1 in undifferentiated wild-type TSCs. Increasing Ovol2 levels suffices to recapitulate the migration phenotype. Furthermore, Lsd1-deficient TSCs exhibit a developmental bias towards cells of the syncytiotrophoblast and impaired spongiotrophoblast and trophoblast giant cell differentiation. In summary, we describe that the epigenetic modifier Lsd1 coordinates placental development by retaining TSCs in their niche and directing trophoblast differentiation. Mouse trophoblast stem cells (TSCs) were isoloated from a single conditional Lsd1-deficient mouse (Lsd1tm1SchM-CM-<le). Deletion of Lsd1 was induced eight days before the collection of RNA by addition of 0.2 M-BM-5M 4OH-tamoxife. Cells were isolated at successive stages of differentiation for total RNA extraction and hybridization on Affymetrix microarrays. To that end, we harvested cells at three time-points: before induction of differentiation (d0), two days after induction of differentiation (d2), and four days after induction of differentiation (d4). Three replicates (1, 2, 3) for control (-) and Lsd1-deficeint (+) cells were included for each differentiation stage.
2014-01-17 | E-GEOD-38277 | biostudies-arrayexpress
Project description:Transitions between pluripotent stem cells and differentiated cells are executed by key transcription regulators. Comparative measurements of RNA polymerase distribution over the genomeM-bM-^@M-^Ys primary transcription units in different cell states can identify the genes and steps in the transcription cycle that are regulated during such transitions. To identify the complete transcriptional profiles of RNA polymerases with high sensitivity and resolution, as well as the critical regulated steps upon which regulatory factors act, we used genome-wide, nuclear run-on (GRO-seq) to map the density and orientation of transcriptionally-engaged RNA polymerases in mouse embryonic stem cells (ESCs) and embryonic fibroblasts (MEFs). In both cell types, progression of a promoter-proximal, paused RNA polymerase II (Pol II) into productive elongation is a rate-limiting step in transcription of ~40% of mRNA-encoding genes. Importantly, quantitative comparisons between cell types reveal that transcription is controlled frequently at paused Pol IIM-bM-^@M-^Ys entry into elongation. Furthermore, M-bM-^@M-^\bivalentM-bM-^@M-^] ESC genes (exhibiting both active and repressive histone modifications) bound by Polycomb Group Complexes PRC 1 and PRC2 show dramatically reduced levels of paused Pol II at promoters relative to an average gene. In contrast, bivalent promoters bound by only PRC2 allow Pol II pausing, but it is confined to extremely 5M-bM-^@M-^Y proximal regions. Altogether, these findings identify rate-limiting targets for transcription regulation during cell differentiation. Mapping engaged RNA polymerase density in two cell types by sequencing run-on transcripts. SUPPLEMENTARY FILES: All fastq files have sanger-fastq format q values. Alignments were generated with eland and the mm9 mouse genome assembly. Reads aligning to regions annotated as similar to rRNA by RepeatMasker were then removed. Wiggle files are in units of RPKM (reads per kilobase per million aligned reads) and are broken up by cell type and chromosome to aid in uploading to UCSC. Each file furthermore contains two tracks - one for each strand. As in the published paper, plus strand RPKM densities are in red with positive values and minus strand RPKM densities are in blue with negative values.
2011-04-01 | E-GEOD-27037 | biostudies-arrayexpress
Project description:Stem cells reside in specific niches providing stemness-maintaining environments. Thus, the regulated migration from these niches is associated with differentiation onset. However, mechanisms retaining stem cells in their niche remain poorly understood. Here, we show that the epigenetic regulator lysine-specific demethylase 1 (Lsd1) organises the trophoblast niche of the early mouse embryo by coordinating migration and invasion of trophoblast stem cells (TSCs). Lsd1 deficiency leads to the depletion of the stem cell pool resulting from precocious migration of TSCs. Migration is induced by premature expression of the transcription factor Ovol2 that is repressed by Lsd1 in undifferentiated wild-type TSCs. Increasing Ovol2 levels suffices to recapitulate the migration phenotype. Furthermore, Lsd1-deficient TSCs exhibit a developmental bias towards cells of the syncytiotrophoblast and impaired spongiotrophoblast and trophoblast giant cell differentiation. In summary, we describe that the epigenetic modifier Lsd1 coordinates placental development by retaining TSCs in their niche and directing trophoblast differentiation.
2014-01-17 | GSE38277 | GEO