Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: phs000249.v1.p1
PROVIDER: PRJNA106863 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome-wide chromatin state maps of murine embryonic stem (ES) cells, ES-derived neural progenitor cells and whole brain tissue. The data were generated to examine the correlation between histone and DNA methylation during lineage-commitment. Keywords: High-throughput ChIP-sequencing, Illumina, cell type comparison H3K4me3, H3K4me2 and/or H3K4me1 ChIP-Seq in singlicate from mouse embryonic stem (ES) cells, ES-derived neural progenitor cells and whole brain tissue suspensions Raw sequence data files for this study are available for download from the SRA FTP site at ftp://ftp.ncbi.nlm.nih.gov/sra/Studies/SRP000/SRP000230
2008-07-05 | E-GEOD-11172 | biostudies-arrayexpress
Project description:Genome-wide chromatin state maps of murine embryonic stem (ES) cells, ES-derived neural progenitor cells and whole brain tissue. The data were generated to examine the correlation between histone and DNA methylation during lineage-commitment. Keywords: High-throughput ChIP-sequencing, Illumina, cell type comparison
2008-07-06 | GSE11172 | GEO
Project description:Genome-wide maps of chromatin state (H3K4me3, H3K9me3, H3K27me3, H3K36me3, H4K20me3) in pluripotent and lineage-committed cells We report the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in mammalian cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse embryonic stem cells, neural progenitor cells and embryonic fibroblasts. We find that lysine 4 and lysine 27 trimethylation effectively discriminates genes that are expressed, poised for expression, or stably repressed, and therefore reflect cell state and lineage potential. Lysine 36 trimethylation marks primary coding and non-coding transcripts, facilitating gene annotation. Trimethylation of lysine 9 and lysine 20 is detected at satellite, telomeric and active long-terminal repeats, and can spread into proximal unique sequences. Lysine 4 and lysine 9 trimethylation marks imprinting control regions. Finally, we show that chromatin state can be read in an allele-specific manner by using single nucleotide polymorphisms. This study provides a framework for the application of comprehensive chromatin profiling towards characterization of diverse mammalian cell populations. Histone H3 or H4 tri-methylation ChIP-Seq in singlicate from murine embryonic stem (ES) cells, ES-derived neural precursor cells, and embryonic fibroblasts.
2008-07-24 | E-GEOD-12241 | biostudies-arrayexpress
Project description:The pluripotent genome is folded in a hierarchy of sophisticated topologies that markedly reconfigure during cell fate transitions. A critical unknown is whether chromatin folding is reversible and functionally linked to the re-establishment of pluripotency in somatic cell reprogramming. Here we integrate classic epigenetic marks with high-resolution architecture maps in embryonic stem (ES) cells, ES-derived neural progenitor cells (NPCs) and NPC-derived induced pluripotent stem (iPS) cells. Collectively we demonstrate that chromatin architecture is only partially reconfigured during somatic cell reprogramming and that pluripotent elements can retain architectural memory from their somatic cell of origin.
2016-05-05 | GSE68582 | GEO
Project description:Understanding the topological configurations of chromatin can reveal valuable insights into how the genome and epigenome act in concert to control cell fate during development. Here we generate high-resolution architecture maps across seven genomic loci in embryonic stem cells and neural progenitor cells. We observe a hierarchy of 3-D interactions that undergo marked reorganization at the sub-Mb scale during differentiation. Distinct combinations of CTCF, Mediator, and cohesin show widespread enrichment in architecture at different length scales. CTCF/cohesin anchor long-range constitutive interactions that might form the topological basis for invariant sub-domains. Conversely, Mediator/cohesin together with pioneer factors bridge short-range enhancer-promoter interactions within and between larger sub-domains. Knockdown of Smc1 or Med12 in ES cells results in disruption of spatial architecture and down-regulation of genes found in cohesin-mediated interactions. We conclude that cell type-specific chromatin organization occurs at the sub-Mb scale and that architectural proteins shape the genome in hierarchical length scales. Analysis of higher-order chromatin chromatin architecture in mouse ES cells and ES-derived NPCs. Analysis of CTCF and Smc1 occupied sites in ES-derived NPCs.
2013-05-24 | E-GEOD-36203 | biostudies-arrayexpress
Project description:A key question in developmental biology is how cellular differentiation is controlled during development. Particular interest has focused upon changes in chromatin state, with transitions between Trithorax-group (TrxG) and Polycomb-group (PcG) chromatin states shown to be vital for the differentiation of ES cells to multipotent stem cells in culture. However, little is known as to the role of chromatin states during the development of complex organs such as the brain. Recent research has also suggested a number of other chromatin states exist in cell culture, including an active state lacking TrxG proteins and a repressive “Black”, “Basal” or “Null” chromatin state devoid of common chromatin marks. The role that these new chromatin states play during development is unknown. Here we show that large scale chromatin remodeling occurs during in vivo Drosophila melanogaster neural development. We demonstrate that the majority of genes that are activated during neuronal differentiation are repressed by the Null chromatin state and a novel TrxG-repressive state in neural stem cells (NSCs). Furthermore, almost all key NSC genes are switched off via a direct transition to HP1-mediated repression. In contrast to previous studies of ES cell to neural progenitor cell development, PcG-mediated repression does not play a significant role in regulating either of these transitions; instead, PcG chromatin specifically regulates lineage-specific transcription factors that control the spatial and temporal patterning of the brain. Combined, our data suggest that forms of chromatin other than canonical PcG/TrxG transitions take over key roles during neural development.
2017-11-24 | GSE77860 | GEO
Project description:<p>For the NIH Roadmap Epigenomics project, we applied ChlP-Seq, HTBS and WGBS pipelines to generate comprehensive high-resolution maps of chromatin state and DNA methylation for 100 diverse cell types. Cell types were selected for their biological and medical importance, and for their potential to maximize the comprehensiveness of acquired epigenomic data. They include human ES cells, ES-derived cells, mesenchymal stem cells, reprogrammed stem cells and primary tissues. Comprehensive characterization of epigenetic marks ("the epigenome") is a critical step towards a global understanding of the human genome in health and disease. In this study we provide unprecedented views of the human epigenetic landscape and its variation across cell states, which offer fundamental insight into the functions and interrelationships of epigenetic marks, and provide a framework for future studies of normal and diseased epigenomes.</p> <p><b>The Roadmap Epigenomics Broad cohort is utilized in the following dbGaP sub-study.</b> To view molecular data and derived variables collected in this sub-study, please click on the following sub-study below or in the "Sub-studies" box located on the right hand side of this top-level study page <a href="study.cgi?study_id=phs000700">phs000700</a> the Roadmap Epigenomics Broad cohort. <ul> <li><a href="study.cgi?study_id=phs000610">phs000610</a> RM_Epigenomics_Broad_Alz</li> </ul> </p>
| phs000700 | dbGaP
Project description:Genome-wide maps of chromatin state in wild type and E2A knockout neural progenitor cells
| PRJNA646462 | ENA
Project description:The developing mammalian brain generates a variety of Neural Progenitor Cells (NPCs). Primary NPCs throughout the neuraxis are derived from the ventricular zone. Intermediate progenitor cells (IPCs) are produced uniquely in the telencephalon and contribute extensively to the neurons that comprise the cerebral cortex and basal ganglia. It is known that the fate of the diverse NPC populations is determined by the interplay of transcription factors and regulation by regional humoral cues. However, despite our recent appreciation that nutrient-regulated intracellular metabolic milieu (pO2, energy, and redox state) significantly influence cell fate, an unexplored area is whether NPCs have intrinsic metabolic identity, and if so, the mechanism by which molecular metabolism contributes to brain development.Little is known however, if intrinsic differences in cellular metabolism of regional NPCs make certain NPCs susceptible while others resistant to genetic and environmental insults. We conjectured that regional (fore-and hindbrain) NPCs are metabolically distinct.
2017-06-19 | ST000767 | MetabolomicsWorkbench
Project description:Human pluripotent stem cell derived models that accurately recapitulate neural development in vitro and allow for the generation of specific neuronal subtypes are of major interest to the stem cell and biomedical community. Notch signaling, particularly through the Notch effector HES5, is a major pathway critical for the onset and maintenance of neural progenitor cells (NPCs) in the embryonic and adult nervous system1-3. Use of a HES5 reporter enables the isolation distinct populations of human embryonic stem (ES) cell derived NPCs that represent building blocks of cortical development in vitro4. Here, we report the transcriptional and epigenomic analysis of six consecutive stages of human ES cell differentiation along the neural lineage aimed at modeling key cell fate decisions including specification, expansion and patterning during the ontogeny of neural stem and progenitor cells. In order to dissect the regulatory mechanisms that orchestrate the stage-specific differentiation process we developed a computational framework to infer key regulators of each cell state transition based on the progressive remodeling of the epigenetic landscape and then validated these through a pooled shRNA screen. We were also able to refine our previous observations on epigenetic priming at transcription factor binding sites and show here that they are mediated by combinations of core and stage-specific factors. Taken together, we demonstrate the utility of our reference maps and outline a general framework, not limited to the context of the neural lineage, to dissect regulatory circuits of differentiation.
2014-11-02 | GSE62193 | GEO