Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

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

ABSTRACT: 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

ORGANISM(S): Mus musculus

SUBMITTER: Sandeep Wontakal

PROVIDER: E-GEOD-21950 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

A large gene network in immature erythroid cells is controlled by the myeloid and B cell transcriptional regulator PU.1.

Wontakal Sandeep N SN Guo Xingyi X Will Britta B Shi Minyi M Raha Debasish D Mahajan Milind C MC Weissman Sherman S Snyder Michael M Steidl Ulrich U Zheng Deyou D Skoultchi Arthur I AI

PLoS genetics 20110609 6

PU.1 is a hematopoietic transcription factor that is required for the development of myeloid and B cells. PU.1 is also expressed in erythroid progenitors, where it blocks erythroid differentiation by binding to and inhibiting the main erythroid promoting factor, GATA-1. However, other mechanisms by which PU.1 affects the fate of erythroid progenitors have not been thoroughly explored. Here, we used ChIP-Seq analysis for PU.1 and gene expression profiling in erythroid cells to show that PU.1 regu ...[more]

PMID: 21695229

Publication: 1/2

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Project description:Differentiation of hematopoietic stem cells to red cells requires coordinated expression of numerous erythroid genes. To understand the regulatory mechanisms governing lineage commitment we conducted a high resolution methylomic and transcriptomic analysis of six major stages of human erythroid differentiation. We observed widespread epigenetic differences between early and late stages of erythropoiesis with progressive loss of methylation being the dominant change during differentiation. Gene bodies, intergenic regions and CpG shores were preferentially demethylated during erythropoiesis. Epigenetic changes at transcription factor binding sites correlated significantly with changes in gene expression and were enriched for binding motifs for SCL, MYB, GATA and other factors not previously implicated in erythropoiesis. Demethylation at gene promoters was associated with increased expression of genes, while epigenetic changes at gene bodies correlated inversely with gene expression. Important gene networks encoding erythrocyte membrane proteins, surface receptors and heme synthesis proteins were found to be regulated by DNA methylation. Furthermore, integrative analysis enabled us to identify novel, potential regulatory areas of the genome that underwent differential methylation and correlated with corresponding changes in gene expression, as evident by epigenetic changes in a predicted PU.1 binding site in intron 1 of the GATA1 gene. This intronic site was found to be conserved across species and was validated to be a novel PU.1 binding site by qCHIP in erythroid cells. Altogether, our study provides a comprehensive analysis of methylomic and transcriptomic changes during erythroid differentiation and demonstrates that hypomethylation of the genome during erythroid differentiation has implications in modulating gene expression. We examined changes in methylation on days 0, 3, 7, 10, 13 and 16 of human erythroid culture. Two independent sets of experiments were performed.

Dataset Information

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

Publications

A large gene network in immature erythroid cells is controlled by the myeloid and B cell transcriptional regulator PU.1.

Similar Datasets

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