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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Enhancer landscape of mouse developing midbrain at 11.5 dpc embryos

ABSTRACT: We report the distribution of histone H3K4me1 and H3K27ac within the genome of mouse embryonic midbrain. We prepared the chromatin from 11 dpc embryonic midbrain and made chromatin precipitation with antibody against H3K4me1 and H3K27ac (rabbit polyclonal antibody). High-throughput sequencing applied for the ChIP analysis revealed the differential distribution of modified histone within developing midbrain. ChIP analysis of mouse 11 dpc embryonic midbrain and forelimb buds against anti-H3K4me1 and H3K27ac antibody.

ORGANISM(S): Mus musculus

SUBMITTER: Takaho Endo

PROVIDER: E-GEOD-49652 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Polycomb potentiates meis2 activation in midbrain by mediating interaction of the promoter with a tissue-specific enhancer.

Kondo Takashi T Isono Kyoichi K Kondo Kaori K Endo Takaho A TA Itohara Shigeyoshi S Vidal Miguel M Koseki Haruhiko H

Developmental cell 20131226 1

Polycomb-group (PcG) proteins mediate repression of developmental regulators in a reversible manner, contributing to their spatiotemporally regulated expression. However, it is poorly understood how PcG-repressed genes are activated by developmental cues. Here, we used the mouse Meis2 gene as a model to identify a role of a tissue-specific enhancer in removing PcG from the promoter. Meis2 repression in early development depends on binding of RING1B, an essential E3 component of PcG, to its promo ...[more]

PMID: 24374176

Similar Datasets

Enhancer landscape of mouse developing midbrain at 11.5 dpc embryos

Project description:We report the distribution of histone H3K4me1 and H3K27ac within the genome of mouse embryonic midbrain. We prepared the chromatin from 11 dpc embryonic midbrain and made chromatin precipitation with antibody against H3K4me1 and H3K27ac (rabbit polyclonal antibody). High-throughput sequencing applied for the ChIP analysis revealed the differential distribution of modified histone within developing midbrain.

2014-01-15 | GSE49652 | GEO

Enhancer landscape of mouse developing forebrain at 11.5 dpc embryos [ChIP-seq]

Project description:We report the distribution of histone H3K4me1 and H3K27ac within the genome of mouse embryonic forebrain. We prepared the chromatin from 11 dpc embryonic forebrain and made chromatin precipitation with antibody against H3K4me1 and H3K27ac (rabbit polyclonal antibody). High-throughput sequencing applied for the ChIP analysis revealed the differential distribution of modified histone within developing forebrain.

2014-11-12 | GSE52280 | GEO

RING1B binding in the 11 dpc embryonic tissues

Project description:We report the distribution of RING1B (one of Polycomb group factors) within the genome of mouse embryonic tissues. We prepared the chromatin from 11 dpc embryonic forebrain, midbrain, and forelimb buds and made chromatin precipitation with antibody against RING1B (mouse monoclonal antibody). High-throughput sequencing applied for the ChIP analysis revealed the differential distribution of RING1B protein among embryonic tissues. ChIP analysis of mouse 11 dpc embryonic forebrain, midbrain and forelimb buds against anti-RING1B antibody.

2014-01-14 | E-GEOD-48464 | biostudies-arrayexpress

RING1B binding in the 11 dpc embryonic tissues

2014-01-14 | GSE48464 | GEO

Regulation of Promoter and Enhancer Histone Landscape by DNA Methylation in Embryonic Stem Cells (ChIP-seq)

Project description:In this study, we mapped modification of lysine 4 and lysine 27 of histone H3 genome-wide in a series of mouse embryonic stem cells (mESCs) varying in DNA methylation levels based on knock-out and reconstitution of DNA methyltransferases (DNMTs). We extend previous studies showing cross-talk between DNA methylation and histone modifications by examining a breadth of histone modifications, causal relationships, and direct effects. Our data shows a causal regulation of H3K27me3 at gene promoters as well as H3K27ac and H3K27me3 at tissue-specific enhancers. We also identify isoform differences between DNMT family members. This study provides a comprehensive resource for the study of the complex interplay between DNA methylation and histone modification landscape. Histone ChIP-seq of H3K4me3, H3K27me3, H3K4me1, and H3K27ac were performed on wild-type, Dnmt triple knock-out (Dnmt1/3a/3b; TKO), Dnmt double knock-out (Dnmt3a/3b; DKO), and respective reconstitution mouse embryonic stem cell lines

2016-08-02 | E-GEOD-77002 | biostudies-arrayexpress

Genome-wide analysis of histone modification, protein-DNA binding, cytosine methylation and transcriptome data in mouse and human ES cells and pig iPS cells

Project description:Genome-wide analysis of histone modification (H2AZ, H3K27ac, H3K27me3, H3K36me3, H3K4me1, H3K4me2, H3K4me3 and H3K9me3), protein-DNA binding (TAF1, P300, Pou5f1 and Nanog), cytosine methylation and transcriptome data in mouse and human ES cells and pig iPS cells We generated histone modification data (H2AZ, H3K27ac, H3K27me3, H3K36me3, H3K4me1, H3K4me2, H3K4me3 and H3K9me3) and protein-DNA binding data (TAF1, P300, Pou5f1 and Nanog) using Chromatin Immunoprecipitation followed by short sequencing (ChIP-seq), cytosine methylation data using methylated DNA immunoprecipitation followed by sequencing (MeDIP-seq) and DNA digestion by methyl-sensitive restriction enzymes followed by sequencing (MRE-seq), transcriptome data with RNA short sequencing (RNA-seq) in human embryonic stem cells, mouse embryonic stem cells, pig induced pluripotent stem cells and mouse embryonic stem cells under activin-A-induced-differentiation. Examination of 8 histone modifications, 4 protein-DNA binding, cytosine methylation and transcriptome in human embryonic stem cells, mouse embryonic stem cells, pig induced pluripotent stem cells and mouse embryonic stem cells under activin-A-induced-differentiation.

2012-02-28 | E-GEOD-36114 | biostudies-arrayexpress

Dynamics of enhancer chromatin signatures mark the transition from pluripotency to cell specification during embryogenesis

Project description:The generation of distinctive cell types that form different tissues and organs requires precise, temporal and spatial control of gene expression. This depends on specific cis-regulatory elements distributed in the non-coding DNA surrounding their target genes. Studies performed on mammalian embryonic stem cells and Drosophila embryos suggest that active enhancers form part of a defined chromatin landscape marked by histone H3 lysine 4 mono-methylation (H3K4me1) and histone H3 lysine 27 acetylation (H3K27ac). Nevertheless, little is known about the dynamics and the potential roles of these marks during vertebrate embryogenesis. Here we provide genomic maps of H3K4me1/me3 and H3K27ac at four developmental time-points of zebrafish embryogenesis and analyze embryonic enhancer activity. We find that: (i) changes in H3K27ac enrichment at enhancers accompany the shift from pluripotency to tissue-specific gene expression; (ii) in early embryos, the peaks of H3K27ac enrichment are bound by pluripotent factors such as Nanog; (iii) the degree of evolutionary conservation is higher for enhancers that become marked by H3K27ac at the end of gastrulation suggesting their implication in the establishment of the most conserved (phylotypic) transcriptome that is known to occur later at the pharyngula stage. ChIP-seq analysis of H3K4me3, H3K4me1 and H3K27ac at four developmental time-points (dome, 80% epiboly, 24hpf and 48pf) of zebrafish embryogenesis.

2012-05-08 | E-GEOD-32483 | biostudies-arrayexpress

Identification of enhancers in EMT and breast cancer stem cell formation

Project description:Epithelial-mesenchymal transition (EMT), the process whereby cells gain migratory and invasive properties characteristic of mesenchymal cells, plays a central role in embryogenesis and wound healing in a wide range of tissues. However, EMT has also been linked to the formation of cancer stem cells (CSCs). Many of the signaling pathways involved in EMT have also been implicated in CSC formation but the processes that contribute uniquely to CSC formation remain elusive. We have previously demonstrated that PKCÎ¸ activation is critical for EMT induction and concomitant CSC formation in the breast cancer luminal epithelial cell line, MCF7. To discover how PKC-induced alterations in the epigenome influence the EMT and CSC formation in MCF-7 cells and MDA-MB-231, we employed a combination of expression profiling and ChIP-sequencing of H3K4me1 and H3K27ac. 3 biological samples were analyzed with two different chromatin marks.

2016-03-10 | E-GEOD-76732 | biostudies-arrayexpress

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [ChIP-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. ChIP-seq with Scl, Hand1, Lsd1, Ezh2, H3K4me1 and H3K27ac in different cell types with mesodermal origin. Scl ChIP-seq in WT, SclKO, SclKO-iScl and Gata12KO mES cell derived day4 EB (embryoid body) Flk1+ mesodermal cells, SclKO-iScl ES cells and MEL cells; Hand1 ChIP-seq in WT mES cell derived day4 EB Flk1+ mesodermal cells; Lsd1 and Ezh2 ChIP-seq in WT and SclKO mES cell derived day4 EB Flk1+ mesodermal cells. ChIP-seq of histone modifications H3K4me1 and H3K27ac in WT, SclKO and Gata12KO mES cell derived day4 EB Flk1+ mesodermal cells, HPC7 hematopoietic progenitor cells and HL1 cardiomyogenic cells

2015-01-01 | E-GEOD-47082 | biostudies-arrayexpress

Batf3 maintains Irf8 autoactivation for commitment of a novel clonogenic progenitor of CD8+DCs

Project description:The transcription factors Batf3 and IRF8 are required for development of CD8α+ conventional dendritic cells (cDCs), but the basis for their actions was unclear. Here, we identify two novel Zbtb46+ progenitors that separately generate CD8α+ and CD4+ cDCs and arise directly from the common DC progenitor (CDP). Irf8 expression in the CDP depends on prior PU.1-dependent autoactivation, and specification of pre-CD8 DC progenitors requires IRF8 but not Batf3. However, upon pre-CD8 DC specification, Irf8 autoactivation becomes Batf3-dependent at a CD8α+ cDC-specific enhancer containing multiple AP1-IRF composite elements (AICEs) within the Irf8 superenhancer. CDPs from Batf3-/- mice that specify toward pre-CD8 DCs fail to complete CD8α+ cDC development due to decay of Irf8 autoactivation, and divert to the CD4+ cDC lineage. Examination of histone modifications (H3K27ac and H3K4me1) and 2 transcription factors (Batf3 and Irf8) and the p300 co-factor binding in 3 different dendritic cell subsets

2015-06-08 | E-GEOD-66899 | biostudies-arrayexpress

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