Genome-wide maps of transcriptional factor binding in mouse erythroid cells.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE47492 | GEO | 2013/12/21
SECONDARY ACCESSION(S): PRJNA207667
REPOSITORIES: GEO
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Project description:Regions bound by the erythroid transcription factors GATA1 and NFE2 and the general factor CTCF were identified in mouse erythroid cells using ChIP-seq. Chip-seq experiements were performed in mouse erythroid Ter119+ cells.
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Project description:Erythropoiesis is dependent on the activity of transcription factors, including the erythroid-specific erythroid Kruppel-like factor (EKLF). ChIP followed by massively parallel sequencing (ChIP-Seq) is a powerful, unbiased method to map transfactor occupancy. We used ChIP-Seq to study the interactome of EKLF in mouse erythroid progenitor cells and more differentiated erythroblasts. We correlated these results with the nuclear distribution of EKLF, RNA-Seq analysis of the transcriptome, and the occupancy of other erythroid transcription factors. In progenitor cells, EKLF is found predominantly at the periphery of the nucleus, where EKLF primarily occupies the promoter regions of genes and acts as a transcriptional activator. In erythroblasts, EKLF is distributed throughout the nucleus, and erythroblast-specific EKLF occupancy is predominantly in intragenic regions. In progenitor cells, EKLF modulates general cell growth and cell cycle regulatory pathways, whereas in erythroblasts EKLF is associated with repression of these pathways. The EKLF interactome shows very little overlap with the interactomes of GATA1, GATA2, or TAL1, leading to a model in which EKLF directs programs that are independent of those regulated by the GATA factors or TAL1. (Blood.2011;118(17):e139-e148) We used ChIP-Seq to study the interactome of EKLF in mouse erythroid progenitor cells and more differentiated erythroblasts and RNA-Seq analysis of the transcriptome.
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Project description:Nuclear receptor binding SET domain protein 1 (NSD1) is recurrently mutated in human cancers including acute leukemia. We found that NSD1 knockdown altered erythroid clonogenic growth of human CD34+ hematopoietic cells. Ablation of Nsd1 in the hematopoietic system induced a transplantable erythroleukemia in mice. Despite abundant expression of the transcriptional master regulator GATA1, in vitro differentiation of Nsd1-/- erythroblasts was majorly impaired associated with reduced activation of GATA1-induced targets, while GATA1-repressed target genes were less affected. Retroviral expression of wildtype Nsd1, but not a catalytically-inactive Nsd1N1918Q SET-domain mutant induced terminal maturation of Nsd1-/- erythroblasts. Despite similar GATA1 levels, exogenous Nsd1 but not Nsd1N1918Q significantly increased GATA1 chromatin occupancy and target gene activation. Notably, Nsd1 expression reduced the association of GATA1 with the co-repressor SKI, and knockdown of SKI induced differentiation of Nsd1-/- erythroblasts. Collectively, we identified the NSD1 methyltransferase as a novel regulator of GATA1-controlled erythroid differentiation and leukemogenesis.
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Project description:RP-LC-MS lipidomics data was collected to understand the role of GATA1 during erythroid maturation. GATA1 mutants and WT cells were treated with or without beta-estradiol. GATA1 mutant cells were additionally treated with or without 5-ALA.
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Project description:Erythropoiesis is dependent on the activity of transcription factors, including the erythroid-specific erythroid Kruppel-like factor (EKLF). ChIP followed by massively parallel sequencing (ChIP-Seq) is a powerful, unbiased method to map transfactor occupancy. We used ChIP-Seq to study the interactome of EKLF in mouse erythroid progenitor cells and more differentiated erythroblasts. We correlated these results with the nuclear distribution of EKLF, RNA-Seq analysis of the transcriptome, and the occupancy of other erythroid transcription factors. In progenitor cells, EKLF is found predominantly at the periphery of the nucleus, where EKLF primarily occupies the promoter regions of genes and acts as a transcriptional activator. In erythroblasts, EKLF is distributed throughout the nucleus, and erythroblast-specific EKLF occupancy is predominantly in intragenic regions. In progenitor cells, EKLF modulates general cell growth and cell cycle regulatory pathways, whereas in erythroblasts EKLF is associated with repression of these pathways. The EKLF interactome shows very little overlap with the interactomes of GATA1, GATA2, or TAL1, leading to a model in which EKLF directs programs that are independent of those regulated by the GATA factors or TAL1. (Blood.2011;118(17):e139-e148)
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Project description:Mammalian erythroid cells development can be divided into three period: hematopoietic stem and progenitor cells (HSPC), erythroid progenitor (Ery-Pro) and erythroid precursor (Ery-Pre). To better understand human erythropoiesis and its regulation, we performed genome-wide studies of chromatin architecture, enhancer and select transcription factors binding, and transcriptomics profiling utilizing modified strategy to obtain defined progenitor and precursor populations from primary human erythroid cells. Integration and analysis of these data reveals that the TAD structure is stable but promoter - enhancer interactions are highly dynamic in a stage specific manner. Erythroid master regulator - GATA1 involves in the P-E interactions stepwisely. GATA1 binding is largely stable in erythroid progenitor and precursor, but dynamic GATA1 binding during this process regulate a productive erythroid gene expression and local chromatin rewiring. Additionally, we also have showed that dosage of GATA1 control the erythroid progenitor behavior and the erythroid progression. The valuable chromatin architecture and epigenome data will provide more comprehensive insight of human erythropoiesis and dynamic gene regulation of cellular differentiation even more broadly.
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Project description:Mammalian erythroid cells development can be divided into three period: hematopoietic stem and progenitor cells (HSPC), erythroid progenitor (Ery-Pro) and erythroid precursor (Ery-Pre). To better understand human erythropoiesis and its regulation, we performed genome-wide studies of chromatin architecture, enhancer and select transcription factors binding, and transcriptomics profiling utilizing modified strategy to obtain defined progenitor and precursor populations from primary human erythroid cells. Integration and analysis of these data reveals that the TAD structure is stable but promoter - enhancer interactions are highly dynamic in a stage specific manner. Erythroid master regulator - GATA1 involves in the P-E interactions stepwisely. GATA1 binding is largely stable in erythroid progenitor and precursor, but dynamic GATA1 binding during this process regulate a productive erythroid gene expression and local chromatin rewiring. Additionally, we also have showed that dosage of GATA1 control the erythroid progenitor behavior and the erythroid progression. The valuable chromatin architecture and epigenome data will provide more comprehensive insight of human erythropoiesis and dynamic gene regulation of cellular differentiation even more broadly.
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Project description:Identification of cell-type specific enhancers is important for understanding the regulation of programs controlling cellular development and differentiation. Enhancers are typically marked by the co-transcriptional activator protein p300 or by groups of cell-expressed transcription factors. We hypothesized that a unique set of enhancers regulates gene expression in human erythroid cells, a highly specialized cell type evolved to provide adequate amounts of oxygen throughout the body. Using chromatin immunoprecipitation followed by massively parallel sequencing, genome-wide maps of candidate enhancers were constructed for p300 and four transcription factors, GATA1, NF-E2, KLF1, and SCL, using primary human erythroid cells. These data were combined with gene expression analyses and candidate enhancers identified. Consistent with their predicted function as candidate enhancers, there was statistically significant enrichment of p300 and combinations of co-localizing erythroid transcription factors within 1-50 kb of the TSS of genes highly expressed in erythroid cells. Candidate enhancers were also enriched near genes with known erythroid cell function or erythroid cell phenotypes. Candidate enhancers exhibited only moderate conservation with mouse and minimal conservation with nonplacental vertebrates. Candidate enhancers were mapped to a data set of erythroid-associated, biologically relevant, SNPs from the GWAS catalog of the NHGRI. Fourteen candidate enhancers, representing 10 genetic loci, mapped to sites associated with biologically relevant erythroid traits. Fragments from these loci directed statistically significant expression in reporter gene assays. Identification of enhancers in human erythroid cells will allow a better understanding of erythroid cell development, differentiation, structure, and function, and provide insights into inherited and acquired hematologic disease. CD34+-selected stem and progenitor cells were expanded for three days in the absence of EPO. The cells were further cultured in the presence of EPO, and formaldehyde crosslinked chromatin was isolated after cells differentiated into R3/R4 nucleated erythroid cells. Chromatin Immunoprecipitation followed by sequencing (chIP-seq) was performed using antibodies against GATA1, KLF1, NFE2, TAL1, p300, H3K4me2 and H3K4me3, along with a total input control. Raw data (fastq, SRA) is missing for the TAL1 chIP-seq dataset
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Project description:Mammalian erythroid cells development can be divided into three period: hematopoietic stem and progenitor cells (HSPC), erythroid progenitor (Ery-Pro) and erythroid precursor (Ery-Pre). To better understand human erythropoiesis and its regulation, we performed genome-wide studies of chromatin architecture, enhancer and select transcription factors binding, and transcriptomics profiling utilizing modified strategy to obtain defined progenitor and precursor populations from primary human erythroid cells. Integration and analysis of these data reveals that the TAD structure is stable but promoter - enhancer interactions are highly dynamic in a stage specific manner. Erythroid master regulator - GATA1 involves in the P-E interactions stepwisely. GATA1 binding is largely stable in erythroid progenitor and precursor, but dynamic GATA1 binding during this process regulate a productive erythroid gene expression and local chromatin rewiring. Additionally, we also have showed that dosage of GATA1 control the erythroid progenitor behavior and the erythroid progression. The valuable chromatin architecture and epigenome data will provide more comprehensive insight of human erythropoiesis and dynamic gene regulation of cellular differentiation even more broadly.
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