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Mus musculus

ABSTRACT: Genome-wide chromatin state maps of ES cells, ES-derived neural progenitor cells and brain tissue

OTHER RELATED OMICS DATASETS IN: phs000249.v1.p1

PROVIDER: PRJNA106863 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR002247.fastq.gz	Fastqsanger.gz
	SRR002248.fastq.gz	Fastqsanger.gz
	SRR002249.fastq.gz	Fastqsanger.gz
	SRR002250.fastq.gz	Fastqsanger.gz
	SRR002251.fastq.gz	Fastqsanger.gz

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Genome-wide chromatin state maps of ES cells, ES-derived neural progenitor cells and brain tissue

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

Genome-wide chromatin state maps of ES cells, ES-derived neural progenitor cells and brain tissue

2008-07-06 | GSE11172 | GEO

Genome-wide maps of chromatin state in pluripotent and lineage-committed cells

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

Genome-wide maps of chromatin state in wild type and E2A knockout neural progenitor cells

Project description:Genome-wide maps of chromatin state in wild type and E2A knockout neural progenitor cells

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Genome-wide nucleosome positioning maps from undifferentiated human iPS cells (hIPS) and iPS cells differentiated to neural progenitor cells (NPC).

Project description:We report the application of MNase-seq (Kent, Adams et al. 2011) to construct genome-wide nucleosome maps from human cells. To date, genome-wide changes in chromatin structure that occur during development in human cells have not been investigated widely. We have constructed and compared genome-wide chromatin maps from undifferentiated human iPS cells and and iPS cells differentiated to neural progenitor cells (NPC).

2019-04-24 | GSE117870 | GEO

Mus musculus

Project description:Genome-wide maps of chromatin state in neural stem/progenitor cells (NSC) from mouse neonatal forebrain [ChIP-seq]

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Project description:Genome-wide maps of chromatin state in neural stem/progenitor cells (NSC) from mouse neonatal forebrain [ChIA-PET]

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Chromatin state changes during neural development revealed by in vivo cell-type specific profiling

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.

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2008-07-25 | GSE12241 | GEO

Local Genome Topology Can Exhibit an Incompletely Rewired 3D-Folding State During Somatic Cell Reprogramming

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

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