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Genome-wide occupancy map of GATA-1 in proliferating and differentiating murine ES cell derived erythroid progenitors (ES-EP)

ABSTRACT: We find GATA-1 occupies 6,600 sites in proliferating erythroid progenitors and 10,600 sites in differentiating progenitors. 80-90% of GATA-1 binds within intragenic or intergenic regions, while <20% of GATA-1 is found within 2kb of TSS. Assaying GATA-1 occupancy in normal erythroid progenitors in both proliferating and differentiating conditions.

ORGANISM(S): Mus musculus

SUBMITTER: Sandeep Wontakal

PROVIDER: E-GEOD-35379 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A core erythroid transcriptional network is repressed by a master regulator of myelo-lymphoid differentiation.

Wontakal Sandeep N SN Guo Xingyi X Smith Cameron C MacCarthy Thomas T Bresnick Emery H EH Bergman Aviv A Snyder Michael P MP Weissman Sherman M SM Zheng Deyou D Skoultchi Arthur I AI

Proceedings of the National Academy of Sciences of the United States of America 20120222 10

Two mechanisms that play important roles in cell fate decisions are control of a "core transcriptional network" and repression of alternative transcriptional programs by antagonizing transcription factors. Whether these two mechanisms operate together is not known. Here we report that GATA-1, SCL, and Klf1 form an erythroid core transcriptional network by co-occupying >300 genes. Importantly, we find that PU.1, a negative regulator of terminal erythroid differentiation, is a highly integrated co ...[more]

PMID: 22357756

Similar Datasets

GATA-1 in proliferating and differentiating murine ES cell derived erythroid progenitors

Project description:This SuperSeries is composed of the following subset Series: GSE35379: Genome-wide occupancy map of GATA-1 in proliferating and differentiating murine ES cell derived erythroid progenitors (ES-EP) GSE35384: Transcriptome analysis of differentiating normal and leukemic erythroid progenitors Refer to individual Series

2012-02-27 | E-GEOD-35385 | biostudies-arrayexpress

Transcriptome analysis of normal erythroid progenitors and erythroleukemia cells

Project description:We compared the transcriptomes of ES cell derived erythroid progentor cells (ES-EP) and murine erythroleukemia (MEL) cells stably transfected with Gata-1 fused to ER. RNA was isolated from duplicate proliferating cultures of MEL and ES-EP using Affymetrix GeneChip Mouse Gene 1.0 ST.

2011-06-23 | E-GEOD-21949 | biostudies-arrayexpress

Genome-wide binding pattern of PU.1 in normal erythroid progenitors and erythroleukemia cells

Project description:We find that the myeloid master regulatory transcription factor, PU.1, binds to >16,000 sites in both normal and leukemic erythroid cells. Of these bound sites, ~7,000 lie within 2kb of TSS of a gene, suggesting PU.1 may regulate a large number of genes in erythroid cells. Coupling this data with gene expression analysis, we show PU.1 directly regulates several critical signaling pathways in erythroid cells. Assaying PU.1 occupancy in normal and leukemic erythroid cells

2011-06-23 | E-GEOD-21950 | biostudies-arrayexpress

AP-1 family members act at DNA targets in conjunction with Sox9 to promote chondrocyte hypertrophy

Project description:A comprehensive analysis of Sox9 binding profiles in developing chondrocytes identified marked enrichment of an AP-1-like motif (Ohba et al. 2015). Here, we have explored the functional interplay between Sox9 and AP-1 in mammalian chondrocyte development. Among AP-1 family members, Jun and Fosl2 were highly expressed within prehypertrophic and early hypertrophic chondrocytes. Chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) showed a striking overlap in Jun- and Sox9-bound regions throughout the chondrocyte genome, a reflection of direct binding of each factor to target motifs in shared enhancers, and physical interactions of AP-1 with Sox9. In vitro expression analysis indicates that direct co-binding of Sox9 and AP-1 at target motifs enhanced target gene expression, while protein-protein interactions suppressed AP-1- and Sox9-driven transcription. Analysis of prehypertrophic chondrocyte removal of Sox9 demonstrated Sox9 was essential for hypertrophic chondrocyte development, while in vitro and ex vivo analyses showed AP-1 promotes chondrocyte hypertrophy. Sox9 and Jun co-bound and co-activated a Col10a1 enhancer in Sox9 and AP-1 motif-dependent manners consistent with their combined action promoting hypertrophic gene expression. Together, the data support a model where AP-1-family members promote Sox9-action in the transition of chondrocytes to a terminal hypertrophic program. Intersection of ChIP-seq data from Sox9 and AP-1 factor Jun, RNA-seq data from developing rib chondrocytes and Col10a1mCherry positive hypertrophic chondrocytes in neonatal mice to uncover regulation of Sox9 by AP-1 factors during chondrocyte hypertrophy.

2016-02-29 | E-GEOD-73372 | biostudies-arrayexpress

Genome-wide mapping of HIF-2 binding in 786-O clear cell renal carcinoma cells

Project description:Kidney cancer accounts for more than 100,000 deaths per year world-wide. More than 80% are clear cell tumors (ccRCCs) and the majority are associated with loss of function of the von Hippel Lindau (pVHL) tumor suppressor resulting in upregulation of HIF-{alpha} subunits, and activation of HIF-dependent transcriptional pathways. Recent GWAS studies have discovered RCC-susceptibility loci both within EPAS1 (HIF-2{alpha}) and in an intergenic region of unknown function on 11q13.3. As part of an ongoing study to define the direct transcriptional targets of HIF-2 in renal cancer, we undertook a genome-wide analysis of HIF-2-binding sites in pVHL-defective 786-O cells (that lack functional HIF-1{alpha} due to a truncated transcript) using chromatin immunoprecipitation with antibodies directed against HIF-2{alpha} and its dimerization partner HIF-1{beta}, coupled to high-throughput sequencing (ChIP-seq). Amongst approximately 600 pangenomic HIF-2{beta} ChIP signals, we observed strong binding (ranked 12th by peak height) almost precisely coinciding with the RCC predisposition SNP rs7105934 on 11q13.3. We report binding of HIF-2{alpha} and HIF-1{beta} in 786-O clear cell renal carcinoma cells. 3 samples examined, HIF-2{alpha}, HIF-1{beta} and pre-immune control ChIP.

2012-02-01 | E-GEOD-34871 | biostudies-arrayexpress

Genome-wide analysis reveals NRP1 as a critical HIF1-E2F7 target gene in the regulation of motorneuron guidance in vivo

Project description:HIF1 is essential for regulation of the transcriptional response to hypoxia. Recently we showed that the transcriptional repressors E2F7 and E2F8 interact and transcriptionally cooperate with HIF1. Here we further explored this cooperation by performing genome-wide analysis, screening for novel HIF1-E2F7 targets. We show that specifically E2F7 is induced in hypoxia by HIF1. Furthermore, chip-sequencing for E2F7 and HIF1 revealed a large number of common targets of which a subset was also regulated by the complex as examined by microarray analysis. Our data show that the HIF1-E2F7 complex can function both as a repressor or activator. Notably, we identify neuropilin 1 (NRP1) as a novel HIF1-E2F7 target, which is repressed by HIF1-E2F7 in vitro and during zebrafish development, depending on E2F-binding sites present in the NRP1 promoter. In addition we show that regulation of NRP1 by the HIF1-E2F7 complex is required for normal axon guidance of spinal motorneurons in vivo. ChIP-seq analysis of HIF1a and E2F7 binding

2015-12-11 | E-GEOD-66956 | biostudies-arrayexpress

The forkhead transcription factor FOXP1 profile in B-cells and B-cell lymphoma cell lines

Project description:Expression of the forkhead transcription factor FOXP1 is essential for early B cell development, whereas downregulation of FOXP1 at the germinal center (GC) stage is required for GC B cell function. Aberrantly high FOXP1 expression is frequently observed in diffuse large B cell lymphoma (DLBCL) and mucosa-associated lymphoid tissue (MALT) lymphoma, being associated with poor prognosis. Here, by gene expression microarray [GSE51382] and quantitative RT-PCR analysis upon ectopic overexpression of FOXP1 in primary human memory B cells (MBCs) and B-cell lines, combined with chromatin immunoprecipitation-sequencing (ChIP-seq), we established that FOXP1 directly represses expression of PRDM1, IRF4, and XBP1, transcriptional master regulators of plasma cell (PC) differentiation. In accordance, FOXP1 is prominently expressed in primary human naive and MBCs but expression strongly decreases during plasma PC differentiation. Moreover, as compared to IgM+ MBCs, IgG+ MBCs combine lower expression of FOXP1 with an enhanced intrinsic PC differentiation propensity, and constitutive (over)expression of FOXP1 in B cell lines and primary human MBCs represses their ability to differentiate into PCs. Taken together, our data indicate that proper control of FOXP1 expression plays a critical role in PC differentiation, whereas aberrant overexpression of FOXP1 might contribute to lymphomagenesis by blocking terminal B cell differentiation. OXP1 ChIP-seq profile in primary human memory B cells (MBCs) and B-cell lines

2015-05-19 | E-GEOD-69009 | biostudies-arrayexpress

Genome-wide analysis of the role of FOG-1 in GATA-1 chromatin occupancy

Project description:We report ChIP-Seq data for GATA-1 and the FOG-binding mutant of GATA-1 (GATA-1^V205G) in G1ME cells, a Gata1-null cell line with both erythroid and megakaryocytic differentiation potential. We introduced HA-tagged GATA-1 or V205G into G1ME cells via retroviral transduction. The cells were crosslinked at 48h post-transduction, and an HA antibody was used for chromatin immunoprecipitation (ChIP). ChIP and input samples were sequenced on Illumina GAII high-throughput sequencer. The data reveal GATA-1-specific and V205G-specific bidning sites, indicating that FOG-1 both faacilitates and prohibits GATA-1 chromatin occupancy in a context-dependent manner. Examinaton of chromatin occupancy of GATA-1 anda FOG-binding mutant of GATA-1 in G1ME cells cultured in TPO.

2012-07-30 | E-GEOD-35644 | biostudies-arrayexpress

Nfatc1 Orchestrates Aging in Hair Follicle Stem Cells

Project description:Mouse hair follicles undergo synchronized cycles. Cyclical regeneration and hair growth is fueled by hair follicle stem cells (HFSCs). We used ChIP-seq to unfold genome-wide chromatin landscapes of Nfatc1 and dissect the biological relevence of its upstream BMP signaling in HFSC aging. Telogen quiescent hair follicle stem cells (HFSCs) were FACS-purified for ChIP-sequcencing.

2013-11-14 | E-GEOD-52328 | biostudies-arrayexpress

ChIPseq Smad3-JMJD3

Project description:ChIP seq of endogenous Smad3 and JMJD3 proteins in mouse embryonic neural stem cells treated with TGFbeta during 30 minutes. Neural stem cells were treated with TGFbeta during 30 minutes, and then chromatin immunoprecipitation was carried out with specific JMJD3 or Smad3 antibodies. Positive and negative controls for each immunoprecipitation were checked before sequencing. Input was used to normalized the sequencing results.

2011-12-30 | E-MTAB-825 | biostudies-arrayexpress

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