Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA116039 | ENA |
REPOSITORIES: ENA
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Project description:We used microarrays to study the effect of Chd1 loss of function in mouse ES cells. We used ChIP-chip to analyze genome-wide binding of Chd1 in normal ES cells. Mouse Embryonic Stem (ES) cells were infected with a lentiviral vector (pSicoR-mCherry) for expression of a shRNA against Chd1 and GFP (as a control). mCherry-sorted ES cells were plated and individual clones were selected and grown under normal ES cell conditions. 6 ES cell clonal lines were isolated and analyzed along with the parental E14 cell line. The final analysis consisted in 3 control cell lines (E14, E1 and G8) and 4 Chd1-deficient cells (3 different clones using a shRNA sequence #1- C1i5, C1i6 and C1i9; 1 clone using a different shRNA (#4) sequence targeting Chd1- C4i2). RNA samples were isolated from these Chd1-deficient ES cells and control ES cells, and hybridized on Affymetrix chip. For ChIP-chip, parental E14 ES cell line was used.
2009-08-13 | E-GEOD-16462 | biostudies-arrayexpress
Project description:We used microarrays to study the effect of Chd1 loss of function in mouse ES cells. We used ChIP-chip to analyze genome-wide binding of Chd1 in normal ES cells.
2009-08-13 | GSE16462 | GEO
Project description:Stem and progenitor cells undergo a global elevation of nascent transcription, or hypertranscription, during key developmental transitions involving rapid cell proliferation. The chromatin remodeler Chd1 binds to RNA Pol I and II genes and is required for hypertranscription in embryonic stem (ES) cells in vitro and the early post-implantation epiblast in vivo. Biochemically, Chd1 has been shown to facilitate transcription at least in part by removing nucleosomal barriers to elongation, but its mechanism of action in stem cells remains poorly understood. Here we report a novel role for Chd1 in the repair of promoter-proximal endogenous double-stranded DNA breaks (DSBs) in ES cells. An unbiased proteomics approach revealed that Chd1 interacts with several DNA repair factors including ATM, Parp1, Kap1 and Topoisomerase 2. We show that wild-type ES cells display high levels of phosphorylated H2AX and Kap1 at chromatin, notably at rDNA in the nucleolus, in a Chd1-dependent manner. Loss of Chd1 leads to an extensive accumulation of DSBs at Chd1 target Pol II genes and rDNA. Genes prone to DNA breaks in Chd1-null ES cells tend to be longer genes with GC-rich promoters, a more labile nucleosomal structure and roles in chromatin organization, transcription and signaling. These results reveal a vulnerability of hypertranscribing stem cells to endogenous DNA breaks, with important implications for developmental and cancer biology.
2021-06-14 | PXD024604 | Pride
Project description:In order to identify the effects of the knock-down of the gene of interest on the mouse ES transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the knock-down cell line. Transcriptome analysis of the knock-down transgenic mouse ES cell line. The knock-down cell line (shE13) was generated by stably expressing a specific short-hairpin RNA against E13 sequence thus knocking-down E13 expression in parental mouse ES cell line E14Tg2a.4 (E14, Hooper M et al., 1987). The specific mouse gene knocked down in the ES cell line is E130012A19Rik.
2012-12-13 | GSE31165 | GEO
Project description:These data include the genome wide location of different histone modifications by ChIP sequencing in mouse ES cells, and RNA Seq data generated from wild type and EED KO mouse ES cells and knocked down for unrelated protein and Setd2 protein. ChIP-Seq: Immuno-precipitation of formaldehyde cross-linked chromatin prepared from wild type mouse E14 ES cells, wild type E36 ES cells, EED KO E36 ES cells, wild type Embryoid bodies (Ebs), EED KO Embryoid bodies (Ebs EED KO) using specific antibody against different histone modifications. RNA-Seq: Total RNA extracted from wild type E36 ES cells, EED KO E36 ES cells, wild type E36 Embryoid bodies (Ebs), EED KO Embryoid bodies (Ebs EED KO), E14 Ctrl KD, E14 Setd2 KD.
2013-12-05 | E-GEOD-51006 | biostudies-arrayexpress
Project description:Regions of H3.3 binding in WT and ATRX KO mouse ES cells were identified by ChIP seq Chip-seq experiements were performed in WT and ATRX KO E14 mouse ES cells
2015-04-16 | E-GEOD-59270 | biostudies-arrayexpress
Project description:The pluripotent mammalian epiblast undergoes unusually fast cell proliferation. This rapid growth is expected to generate a high transcriptional demand, but the underlying mechanisms remain unknown. We report that the chromatin remodeler Chd1, which binds the activating histone mark H3K4me3 and is associated with transcription, is required for development of the mouse epiblast. Chd1-/- embryos exhibit proliferation defects and increased apoptosis, are smaller than controls by E5.5, and fail to grow, become patterned or gastrulate. We show that Chd1-/- ES cells have a self-renewal defect and a genome-wide reduction in transcriptional output that is associated with losses in RNA Pol II elongation at growth-promoting genes, including ribosomal proteins. We also report that Chd1 directly regulates ribosomal RNA transcription and that both Chd1-/- epiblast cells in vivo and ES cells in vitro express significantly lower levels of ribosomal RNA. Single cell analyses reveal abnormal nucleolar morphology in mutants in vivo and in vitro. These data indicate that Chd1 promotes a globally elevated transcriptional output required to sustain the distinct rapid growth of the mouse epiblast.
2014-12-31 | GSE57609 | GEO
Project description:Analysis of gene expression in Mouse E14-TG2a.IV strain ES cells
2013-12-21 | GSE47757 | GEO
Project description:Transcriptome analysis of Mouse E14-TG2a.IV ES cells
| PRJNA207666 | ENA
Project description:This SuperSeries is composed of the following subset Series: GSE28141: Genome-wide analysis of REST knockdown responsive gene expression in mouse ES cells GSE28233: Genome-wide maps of REST and its cofactors in mouse E14 cells Refer to individual Series
2011-03-31 | E-GEOD-28289 | biostudies-arrayexpress