Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA374841 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Heme and GATA1 coordinately regulate erythroid differentiation [RNA-seq]
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Project description:Heme and GATA1 coordinately regulate erythroid differentiation
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Project description:In mice lacking the heme exporter, FLVCR, differentiation fails at the CFU-E/proerythroblast stage from excessive heme and reactive oxygen species. We show that Flvcr1-deleted CFU-E/proerythroblasts have low GATA1 mRNA and GATA1-target gene mRNAs along with increased ribosomal protein mRNAs as a direct result of increased heme. Thus heme increases ribosomal protein transcription when globin production needs to be increased, and when heme is excessive, GATA1 is reduced allowing for normal termination of erythroid differentiation. This demonstrates that heme and GATA1 are co-master regulators of erythroid differentiation.
2019-02-07 | GSE94905 | GEO
Project description:In mice lacking the heme exporter, FLVCR, differentiation fails at the CFU-E/proerythroblast stage from excessive heme and reactive oxygen species. We show that Flvcr1-deleted CFU-E/proerythroblasts have low GATA1 mRNA and GATA1-target gene mRNAs along with increased ribosomal protein mRNAs as a direct result of increased heme. Thus heme increases ribosomal protein transcription when globin production needs to be increased, and when heme is excessive, GATA1 is reduced allowing for normal termination of erythroid differentiation. This demonstrates that heme and GATA1 are co-master regulators of erythroid differentiation.
2019-02-07 | GSE94898 | GEO
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.
2020-04-08 | PXD017657 | Pride
Project description:GATA-1 and heme regulate the erythroid cell transcriptome.
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Project description:NF45 and NF90/NF110 coordinately regulate ESC pluripotency and differentiation
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Project description:Expression data from G1E erythroid cells expressing GATA1 mutants
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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.
2023-05-07 | GSE214805 | GEO
Project description:CRISPR/Cas9-mediated ablation of two Alas2 intronic cis-elements in G1E-ER-GATA1 cells strongly reduced GATA-1-induced Alas2 transcription, heme biosynthesis, and GATA-1 regulation of other vital constituents of the erythroid cell transcriptome. Bypassing Alas2 function in Alas2 cis-element-mutant (double mutant) cells by providing its catalytic product 5-aminolevulinic acid (5-ALA) rescued heme biosynthesis and a subset of GATA-1-dependent genetic network. Using the same system, we discovered a GATA-1- and heme-dependent circuit that regulates chromatin accessibility during erythroid maturation.
2018-05-30 | GSE114996 | GEO