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MiniChIP-chip of murine hematopoietic stem cells and progeny with H3K4me3, H3K79me2, H3K9/14ac, H3K27me3, H3K9me3, PolII

ABSTRACT: This study describes the changes in epigenetic chromatin modifications during murine hematopoietic stem cell differentiation in vivo using a modified miniChIP-chip technology. We have addressed issues including bivalent (H3K4me3/H3K27me3) modifications, lineage priming hypothesis, and stem cell chromatin properties in our study described in Weishaupt et al., 2009 (Blood)

ORGANISM(S): Mus musculus

PROVIDER: GSE18734 | GEO | 2009/11/09

SECONDARY ACCESSION(S): PRJNA123837

REPOSITORIES: GEO

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miniChIP-chip of murine hematopoietic stem cells and progeny with H3K4me3, H3K79me2, H3K9/14ac, H3K27me3, H3K9me3, PolII

Project description:This study describes the changes in epigenetic chromatin modifications during murine hematopoietic stem cell differentiation in vivo using a modified miniChIP-chip technology. We have addressed issues including bivalent (H3K4me3/H3K27me3) modifications, lineage priming hypothesis, and stem cell chromatin properties in our study described in Weishaupt et al., 2009 (Blood) Comparison of 4 murine hematopoietic stem, progenitor and mature cell types directly isolated from primary tissues using FACS. HSCs are phenotypically identified in bone marrow as lineage-, cKit+, Sca1+, CD150+, Flk2/Flt3- (LSKCD150+ cells). MPPs are phenotypically identified in bone marrow as lineage-, cKit+, Sca1+, CD150-, Flk2/Flt3+ (LSKCD150- cells). PreMegEs are phenotypically identified in bone marrow as lineage-, cKit+, Sca1-, CD150+, CD105-, FcgRI/IIlo and CD41- cells as described in Pronk et al., 2007. Splenic-derived CD4+ T cells are phentypically identified as CD4+, CD8-, B220-, Nk1.1- cells as described in Rolf et al., 2008.

2009-11-08 | E-GEOD-18734 | biostudies-arrayexpress

Temporal dynamics of histone modification H3K9/14ac, H3K27ac, H3K4me3, H3K27me3, and H3K36me3 after wounding in Arabidopsis thaliana.

Project description:After wounding in plants, a vast and rapid transcriptional reprogramming takes place. Interestingly, this reprogramming includes the reactivation of developmental regulators that in mature tissue normally are epigenetically repressed. We evaluated which histone modifications are associated with this rapid increase of these developmental regulators.

2019-11-28 | E-MTAB-7611 | biostudies-arrayexpress

H3K9/14Ac in TC-797 genome

Project description:The goal is to localize "active" histone marks known to bind BRD4-NUT in the NMC genome. Characterization of the reference epigenome in humans by use of ChIP-Seq in the TC-797 human NMC cell line.

2013-03-05 | GSE36512 | GEO

ChIP-seq for H3K4me3, H3K27me3, H3K79me2 in MCF10A cells

Project description:We performed ChIP-Seq against histones H3K4me3, H3K27me3, and H3K79me2 in MCF10A cells to identify transcription factors with bivalent and pseudo-bivalent epigenetic modifications.

2018-02-01 | GSE109721 | GEO

ChIP-on-chip from murine myeloid cell line M1 and virus-induced myeloid leukemia cell lines for H3K4me3, H3K9/14ac, H3K4me1, H3K27me3, H3K9me3 and CTCF

Project description:Histone modifcations and CTCF binding at the c-myb locus were compared in cell lines with c-myb expressing, which are myeloblatic M1 cells and leukemia cells with virus integration, VS. M1 cells without c-myb expression induced by IL-6. Distribution of active histone marks at the c-myb gene and the upstream regions are associated with active c-myb transcription. The enrichment of all of these active histone marks decreased with differentiation-induced down-regulation of c-myb, but increased and spread in tumor cells.

2012-09-01 | GSE34770 | GEO

ChIP-on-chip from murine myeloid cell line M1 and virus-induced myeloid leukemia cell lines for H3K4me3, H3K9/14ac, H3K4me1, H3K27me3, H3K9me3 and CTCF

2012-09-01 | E-GEOD-34770 | biostudies-arrayexpress

H3K9/14Ac in TC-797 genome

2013-03-05 | E-GEOD-36512 | biostudies-arrayexpress

ChIP-Seq sequencing of novel interactors of H3K4me3, H3K36me3 and H3K9me3

Project description:This study describes the epigenetic profiling of the novel interactors of H3K4me3, H3K36me3 or H3K9me3. The interactors were ChIP-Seq profiled by their GFP tag in stably transfected HeLa (Kyoto) cells. The interactors include GATAD1, Sgf29, BAP18, TRRAP, PHF8, N-PAC and LRWD1 (including replicates), as well as an GFP ChIP-Seq profile on non-transfected HeLa cells (negative control). Also included are the profiles of the histone modifications themselves (H3K4me3, H3K27me3, H3K9me3, H3K36me3, H3K9/14Ac and H3K79me3) ChIP-Seq profiling of 8 proteins by their GFP tag in stably transfected cells HeLa (Kyoto) cells, 6 replicas, as well as ChIP-Seq profiling of 6 histone modifications in wt HeLa (Kyoto) cells

2010-09-17 | E-GEOD-20303 | biostudies-arrayexpress

H3K27ac, H3K4me3, H3K27me3 and H3K9me3 ChIPseq of SKOV3(AA) and SKOV3(CC)

Project description:To study the effect of rs1192691 on histone modifications, we performed H3K27ac, H3K4me3, H3K27me3 and H3K9me3 in SKOV3(AA) and SKOV3(CC).

2022-01-18 | GSE182333 | GEO

KDM4A regulates the maternal-to-zygotic transition by protecting broad H3K4me3 domains from H3K9me3 invasion in oocytes.

Project description:The importance of germline-inherited post-translational histone modifications on priming early mammalian development is just emerging1-4. Histone H3 lysine 9 (H3K9) trimethylation is associated with heterochromatin and gene repression during cell-fate change5, whereas histone H3 lysine 4 (H3K4) trimethylation marks active gene promoters6. Mature oocytes are transcriptionally quiescent and possess remarkably broad domains of H3K4me3 (bdH3K4me3)1,2. It is unknown which factors contribute to the maintenance of the bdH3K4me3 landscape. Lysine-specific demethylase 4A (KDM4A) demethylates H3K9me3 at promoters marked by H3K4me3 in actively transcribing somatic cells7. Here, we report that KDM4A-mediated H3K9me3 demethylation at bdH3K4me3 in oocytes is crucial for normal pre-implantation development and zygotic genome activation after fertilization. The loss of KDM4A in oocytes causes aberrant H3K9me3 spreading over bdH3K4me3, resulting in insufficient transcriptional activation of genes, endogenous retroviral elements and chimeric transcripts initiated from long terminal repeats during zygotic genome activation. The catalytic activity of KDM4A is essential for normal epigenetic reprogramming and pre-implantation development. Hence, KDM4A plays a crucial role in preserving the maternal epigenome integrity required for proper zygotic genome activation and transfer of developmental control to the embryo.

| S-EPMC7212036 | biostudies-literature

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