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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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High resolution analysis of epigenetic changes associated with X inactivation, ChIP-Seq

ABSTRACT: This study describes the epigenetic profiling of the X chromosome during X inactivation. It includes H3K4me3 and H3K27me3 ChIP-Seq profiles of male (E14) and female (LF2 and XT67E1) mouse ES cells, together with their differentiated derivatives (either 4d atRA or 10d EB). It also includes ChIP-chip profiles around the Xic on chromosome X of H3K4me3, H3K27me3, H3K9me2, H3K36me3, Pol II, TBP, H3-Core as well as expression, using male (E14) and female (LF2) mouse ES cells, together with their differentiated derivatives (either 4d atRA or 10d EB). Examination of two different histone modifications in 3 cell lines under 3 conditions using ChIP-Seq. Examination of five different histone modifications two transcription factors and gene expression under three conditions in 2 cell lines using ChIP-chip.

ORGANISM(S): Mus musculus

SUBMITTER: H. Stunnenberg

PROVIDER: E-GEOD-15814 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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High-resolution analysis of epigenetic changes associated with X inactivation.

Marks Hendrik H Chow Jennifer C JC Denissov Sergei S Françoijs Kees-Jan KJ Brockdorff Neil N Heard Edith E Stunnenberg Hendrik G HG

Genome research 20090706 8

Differentiation of female murine ES cells triggers silencing of one X chromosome through X-chromosome inactivation (XCI). Immunofluorescence studies showed that soon after Xist RNA coating the inactive X (Xi) undergoes many heterochromatic changes, including the acquisition of H3K27me3. However, the mechanisms that lead to the establishment of heterochromatin remain unclear. We first analyze chromatin changes by ChIP-chip, as well as RNA expression, around the X-inactivation center (Xic) in fema ...[more]

PMID: 19581487

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High resolution analysis of epigenetic changes associated with X inactivation, ChIP-chip

2009-06-06 | GSE15883 | GEO

High resolution analysis of epigenetic changes associated with X inactivation, ChIP-Seq

2009-06-06 | GSE15814 | GEO

High resolution analysis of epigenetic changes associated with X inactivation, ChIP-chip

Project description:This study describes the epigenetic profiling of the X chromosome during X inactivation. It includes H3K4me3 and H3K27me3 ChIP-Seq profiles of male (E14) and female (LF2 and XT67E1) mouse ES cells, together with their differentiated derivatives (either 4d atRA or 10d EB). It also includes ChIP-chip profiles around the Xic on chromosome X of H3K4me3, H3K27me3, H3K9me2, H3K36me3, Pol II, TBP, H3-Core as well as expression, using male (E14) and female (LF2) mouse ES cells, together with their differentiated derivatives (either 4d atRA or 10d EB). Examination of two different histone modifications in 3 cell lines under 3 conditions using ChIP-Seq. Examination of five different histone modifications two transcription factors and gene expression under three conditions in 2 cell lines using ChIP-chip.

2010-05-18 | E-GEOD-15883 | biostudies-arrayexpress

Jarid2 methylation is required for PRC2 functioning during ES cells differentiation

Project description:We report that Jarid2 is methylated at K116 by the polycomb complex PRC2. We analyzed Jarid2 versus Methylated Jarid2 genomic localization by ChIP-seq. We also study H3K27 enrichment in Jarid2 knock out ES cells and in cells rescued for Jarid2 or a mutant that cannot be methylated. ChIP-seq for H3K27me3 was perfomed in undiffrentiated ES cells as well as after 8 days of diffrentiation toward Embroyid Bodies (Hanging Drop method). Experiment 1: Jarid2 vs Jarid2me ChIP-seq in undifferentiated mouse ES cells (E14). Experiment 2: H3K27me3 ChIP-seq in Jarid2 -/- ES cells (peng, 2009, Cell), or the same cells rescue with a BAC expressing JARID2 or a mutant of K116 to A. H3K27me3 Chip-seq were perfomed in undifferentiated ES cells and in EB after 8 days of differentiation (hanging Drop method).

2015-01-22 | E-GEOD-55630 | biostudies-arrayexpress

Comprehensive analysis of genome-wide transcriptome modification during neuronal differentiation of mouse embryonic stem cells by all-trans retinoic acid

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2017-03-01 | GSE93581 | GEO

The effects of oxygen treatments on angiogenesis and lymphangiogenesis in mouse embryoid bodies

Project description:This study investigates the processes of angiogenesis and lymphangiogenesis in an in vitro mouse Embryoid Body (EB) model while maintaining as closely as possible an in vivo environment that is observed in human and murine placental development. Several studies have documented that human placental development is profoundly influenced by oxygen tension. Further the developing murine embryo also experiences hypoxic conditions prior to parturition, which regulates early organogenesis and embryonic blood vessel formation in vivo. Embryonic stem (ES) cells derived from 129/SvJ mice were differentiated into embryoid bodies (EBs) and were subjected to two oxygen treatments: normoxia (21% O2) and hypoxia (2.6%). Hypoxia was achieved in a humidified chamber flushed with 95% N2/5% CO2 until the oxygen level was stably maintained at 2.6%. EBs were transferred on days E8, E12, E15 and E18 to hypoxia or maintained in normoxia. After 2 days of differential oxygen treatments, these EBs were analyzed at E10, E14, E17 and E20 respectively. A 4 x 2, reference-based, experimental design was utilized consisting of 4 timepoints (E10, E14, E17 and E20) subjected to 2 oxygen treatments (normoxia, hypoxia) with n=4 biological replicates present in each group. All EB samples were handled in parallel through all experimental steps. Each EB RNA sample was amplified, labeled with Cy5, and compared to the same Mouse Universal Reference RNA sample (Stratagene, La Jolla, CA) that was amplified and labeled with Cy3 dye. No dye swaps were utilized.

2012-08-11 | E-GEOD-17613 | biostudies-arrayexpress

The PRC2-associated factor C17orf96 is a novel CpG island regulator in mouse ES cells

Project description:CpG islands (CGIs) are key DNA regulatory elements in the vertebrate genome and are often found at gene promoters. In mammalian embryonic stem (ES) cells, CGIs are decorated by either the active or repressive histone marks, H3K4me3 and H3K27me3, respectively, or by both modifications (‘bivalent domains’), but their precise regulation is incompletely understood. Remarkably, we find that the polycomb repressive complex 2 (PRC2)-associated protein C17orf96 (a.k.a. esPRC2p48 and E130012A19Rik) is present at most CGIs in mouse ES cells. At PRC2-rich CGIs, loss of C17orf96 results in an increased chromatin binding of Suz12 and elevated H3K27me3 levels concomitant with gene repression. In contrast, at PRC2-poor CGIs, located at actively transcribed genes, C17orf96 colocalizes with RNA polymerase II and its depletion leads to a focusing of H3K4me3 in the core of CGIs. Our findings thus identify C17orf96 as a novel context-dependent CGI regulator. ChIP-seq of C17orf96, H3K4me3 and H3K27me3 in mouse ES cells (E14).

2015-04-29 | E-GEOD-63491 | biostudies-arrayexpress

Influence of Water Chemistry on Toxicogenomics of Chronic Lead Toxicity to the Fathead Minnow (Pimephales promelas)

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2008-04-06 | E-GEOD-8404 | biostudies-arrayexpress

Polycomb-dependent H3K27me1 and H3K27me2 regulate active transcription and enhancer fidelity

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2013-12-05 | E-GEOD-51006 | biostudies-arrayexpress

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Project description:This experiment sought to determine the chromatin structure and PRC2 occupancy at the promoters of all genes in mouse ESCs ChIP-seq for EZH2, SUZ12, and H3K27me3 were performed on WT E14 cells in 2 biological replicates each. In addition H3K27me3 ChIP-seq was also performed on a clone of E14 cells expressing a tagged version of EZH2, which for the purpose of this study was used as replicate #3.

2013-10-19 | E-GEOD-49431 | biostudies-arrayexpress

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