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Genome-wide maps of H3R2me2s in pro-B cells

ABSTRACT: We report the application of single-molecule-based sequencing technology for high-throughput profiling of H3R2me2s in mouse pro-B cells. We find that H3R2 symmetric dimethylation and H3K4 trimethylation colocalized throughout the genome of mouse pro-B cells. Examination of 2 different histone modifications in mouse pro-B cells

ORGANISM(S): Mus musculus

SUBMITTER: Mark Borowsky

PROVIDER: E-GEOD-35316 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide maps of H3R2me2s in pro-B cells

Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of H3R2me2s in mouse pro-B cells. We find that H3R2 symmetric dimethylation and H3K4 trimethylation colocalized throughout the genome of mouse pro-B cells.

2012-02-02 | GSE35316 | GEO

Essential role of EBF1 in B cell immunity by controlling the generation and function of distinct mature B cell types

Project description:The transcription factor EBF1 is essential for lineage specification in early B cell development. Here we demonstrate by conditional mutagenesis that EBF1 was required for B cell commitment, pro-B cell development and subsequent transition to pre-B cells. Later in B cell development, EBF1 was essential for the generation and maintenance of distinct mature B cell types. Marginal zone and B-1 B cells were lost, whereas follicular and germinal center B cells were reduced in the absence of EBF1. Activation of the B cell receptor resulted in impaired intracellular signaling, proliferation and survival of EBF1-deficient follicular B cells. Immune responses were severely reduced upon Ebf1 inactivation, as germinal centers were formed but not maintained. ChIP- and RNA-sequencing of follicular B cells identified EBF1-activated genes that code for receptors, signal transducers and transcriptional regulators implicated in B cell signaling. Notably, ectopic expression of EBF1 efficiently induced the development of B-1 cells at the expense of conventional B cells. These gain- and loss-of-function analyses uncovered novel important functions of EBF1 in controlling B cell immunity. 29 samples (4 ChIP-seq,16 input, 9 RNA-seq), All ChIP-seq in 2 biological replicates, but EBF1 ChIP-seq Pro-B in 2 technical replicates; All RNA-seq in 2 biological replicates but RNA-seq mature B_FO B_Cd23-Cre Ebf1(fl/–). WT and experimental samples are provided.

2012-03-20 | E-GEOD-35857 | biostudies-arrayexpress

Functional Identification of Critical Bmi1 target genes in Neural Progenitor and Malignant Glioma cells

Project description:In this study, we combined a genome-wide analysis of the Polycomb protein Bmi1 and an in vivo RNAi screening to identify critical targets whose repression in neural progenitor and Malignant Glioma cells enables normal and aberrant self-renewal. Bmi1 ChIP-sequencing generated in 2 primary adult mouse Neural Progenitor cell lines, 1 mouse astrocytic cell line, 1 mouse Glioma initiating cell line, and 1 mouse Glioma cell line. In human cell lines, Bmi1 ChIP-seq was performed for foetal Neural Progenitor Cells, and 2 Glioblastoma Stem-like cells. ChIP-seq for AP-1 in one Glioblastoma stem-like cell line. ChIP-sequencing were generated using either Illumina GxII or HiSeq. We have further performed RNA-seq of adult Ink4a/Arf -/-;BMI1or GFP dox-inducible shRNA mNPC with a doxycycline inducible shRNA targeting BMI1 or GFP (as control). These cells were either treated with doxyclyine for 48h to ablate BMI1 and GFP expression or further subjected to short-term differentiation using either BMP4 (10ng/ml or 50ng/ml for 3 or 6hrs), or FBS (1 or 10% for 3 or 6hrs). Additional mouse RNA-seq were performed in two biological replica of adult mouse brains (littermate) with either wild-type FVB background or BMI1 -/-. Finally, we performed RNA-seq in human Glioblastoma stem-like cells (most likely belonging to the mesenchymal GBM subtype) treated with BMP7, Arvanil and doxycycline or EtOH treated as ctrl.

2013-05-21 | E-GEOD-33912 | biostudies-arrayexpress

Nascent-Seq Reveals Novel Features of Mouse Circadian Transcriptional Regulation

Project description:This SuperSeries is composed of the following subset Series: GSE36871: Nascent-Seq Reveals Novel Features of Mouse Circadian Transcriptional Regulation [RNA-Seq] GSE36872: Nascent-Seq Reveals Novel Features of Mouse Circadian Transcriptional Regulation [Nascent-Seq] GSE36873: Nascent-Seq Reveals Novel Features of Mouse Circadian Transcriptional Regulation [StrandSpe_NascentSeq] GSE36874: Nascent-Seq Reveals Novel Features of Mouse Circadian Transcriptional Regulation [ChIP-seq] Refer to individual Series

2012-11-09 | E-GEOD-36916 | biostudies-arrayexpress

Genome wide mapping of histone acetyltransferase MOF binding in murine ES cells (sequencing)

Project description:We report the application of illumina sequencing technology for high-throughput profiling of histone acetyltransferase Mof in mouse embryonic stem 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. We find that Mof widely binds to mouse genome and mark genes that are expressed, poised for expression, or stably repressed. Mof binds to both gene promoters and coding regions, exhibiting two modes of binding. This study provides a framework for understanding the function of Mof in regulating ESC core transcription network. Examination of Mof binding patterns in ES cells

2012-08-09 | E-GEOD-37268 | biostudies-arrayexpress

Genome-wide transcription factor binding maps of glioma-associated oncogene family zinc finger 3 (Gli3) in Second Heart Field (SHF) cells disected from Mouse Embryos.

Project description:To investigate the heart development, the data were generated to examine the genome-wide Gli3 binding in SHF disected from Mouse Embryos. Gli3 ChIP-Seq was compared to the input in SHF from mouse embryonic cells at E9.5.

2013-03-01 | E-GEOD-44755 | biostudies-arrayexpress

ETS Family Transcriptional Regulators Drive Chromatin Dynamics and Malignancy in Squamous Cell Carcinomas (ChIP-Seq I)

Project description:After characterizing super-enhancer-associated chromatin dynamics accompanied by malignant progression of skin stem cells, we show that ETS family members auto-regulate themselves and a cohort of cancer-associated super-enhancer transcription factors which together are essential for tumor maintenance. Mouse skin squamouse cell carcinoma (SCC) tumor-initiating stem cells (SCs) were FACS-purified for ChIP-sequencing.

2015-11-22 | E-GEOD-72145 | biostudies-arrayexpress

Estrogen Receptor alpha ChIP-Seq in mouse mammary gland

Project description:Estrogen Receptor is a key transcriptional regulator in mammary gland development and breast cancer. In this study, we have mapped the Estrogen Receptor chromatin binding patterns in healthy mouse mammary gland A minimum of 6 pairs of mouse mammary gland pads from mice at 5-6 weeks of age were excised and Estrogen Receptor ChIp-seq was performed.

2013-01-11 | E-GEOD-43415 | biostudies-arrayexpress

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

Brg1 activates enhancer repertoires to establish B cell identity and modulate cell growth

Project description:Early B cell development is orchestrated by the combined activities of the transcriptional regulators E2A, EBF1, Foxo1 and Ikaros. However, how the genome-wide binding patterns of these regulators are modulated during B-lineage development remains to be determined. Here, we found that in lymphoid progenitors the chromatin remodeler Brg1 specified the B cell fate. In committed pro-B cells Brg1 regulated Igh locus contraction and controlled c-Myc expression to modulate the expression of genes that regulate ribosome biogenesis. In committed pro-B cells Brg1 also suppressed a pre-B lineage-specific pattern of gene expression. Finally, we found that Brg1 acted mechanistically to establish B cell fate and modulate cell growth by facilitating access of lineage-specific transcription factors to poised enhancer repertoires. 8 ATAC-Seq samples from sorted ALP and BLP (duplicates, control and Brg1-deleted), 4 ATAC-Seq samples from cultured pro-B cells (duplicates, control and Brg1-deleted), 2 Ikaros ChIP-seq samples (performed in Rag1-/- pro-B cells and in E2A-/- pre-pro-B cells), 1 Brg1 ChIP-seq sample and accompanying Input sample (both in Rag1-/- pro-B cells), 4 RNA-Seq samples from cultured pro-B cells (duplicates, control and Brg1-deleted), 6 RNA-Seq samples from cultured Rag1-/- pro-B cells (triplicates, control and Brg1-knock down).

2015-05-15 | E-GEOD-66978 | biostudies-arrayexpress

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