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The NFIA-ETO2 fusion blocks terminal erythroid maturation and induces pure erythroid leukemia (PEL)

ABSTRACT: The NFIA-ETO2 fusion is the product of a t(1;16)(p31;q24) chromosomal translocation so far exclusively found in pediatric patients with pure erythroid leukemia (PEL). To address its role for the pathogenesis of the pure erythroid leukemia, we retrovirally expressed the PEL-associated NFIA-ETO2 fusion in primary erythroblasts in fetal liver-derived erythroblasts from wild-type (C57/B6) mice. To better characterize alteration in chromatin accessibility due to NFIA-ETO2 expression, we analyzed accessible chromatin state by ATAC sequencing from cells kept in 24h in differentiation-inducing medium (DM)

ORGANISM(S): Mus musculus

PROVIDER: GSE205392 | GEO | 2023/02/08

REPOSITORIES: GEO

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The NFIA-ETO2 fusion blocks terminal erythroid maturation and induces pure erythroid leukemia (PEL) in cooperation with mutant TP53

Project description:The NFIA-ETO2 fusion is the product of a t(1;16)(p31;q24) chromosomal translocation so far exclusively found in pediatric patients with pure erythroid leukemia (PEL). To address its role for the pathogenesis of the pure erythroid leukemia, we retrovirally expressed the PEL-associated NFIA-ETO2 fusion or an in active NFIA-ETOdeltaNHR4 mutant in primary erythroblasts in fetal liver-derived erythroblasts from either wild-type (C57/B6) or TP53R248Q (HUPKI) mice. Gene expression was determined by RNA sequencing from cells kept in maintenance medium (MM) or 24h in differentiation-inducing medium (DM)

2023-02-09 | GSE205420 | GEO

Effect of NFIA-ETO2 gene fusion on MEL cells during proliferation and impaired erythroid differentiation.

2023-02-09 | GSE205407 | GEO

Location of NFIA-ETO2 binding site on genome in MEL cells

Project description:The NFIA-ETO2 fusion is the product of a t(1;16)(p31;q24) chromosomal translocation so far exclusively found in pediatric patients with pure erythroid leukemia (PEL). To address its role for the pathogenesis of the pure erythroid leukemia, we retrovirally expressed the PEL-associated NFIA-ETO2 fusion in MEL cells. To better identify direct target gene loci, we sequenced NFIA-ETO2-associated immunoprecipitated chromatin and histone modifications.

2023-02-09 | GSE205397 | GEO

Expression data from ETO2 knockdown G1E-ER-GATA-1 cells

Project description:We used microarrays to examine what genes could be regulated by ETO2 in erythroid cells. Comparing expression profile in murine G1E-ER-GATA-1 cells treated with control and ETO2(Cbfa2t3) siRNA on Agilent array. After siRNA transfection, the cells were treated with b-estradiol for 24h to induce GATA-1-mediated erythroid maturation.

2010-09-25 | E-GEOD-24333 | biostudies-arrayexpress

Expression data from ETO2 knockdown G1E-ER-GATA-1 cells

Project description:We used microarrays to examine what genes could be regulated by ETO2 in erythroid cells.

2010-09-25 | GSE24333 | GEO

Distinct Ldb1/NLI complexes orchestrate γ-globin repression and re-activation through ETO2 in human adult erythroid cells.

Project description:The Ldb1/GATA-1/TAL1/LMO2 complex mediates long range interaction between the β-globin locus control region (LCR) and gene in adult mouse erythroid cells but whether this complex mediates chromatin interactions at other developmental stages or in human cells is unknown. We investigated human NLI (Ldb1 homologue) complex occupancy and chromatin conformation of the β-globin locus in human erythroid cells. In addition to the LCR, we find robust NLI complex occupancy at a site downstream of the Aγ-globin gene, within sequences of BGL3, an intergenic RNA transcript. In cells primarily transcribing β-globin, BGL3 is not transcribed and BGL3 sequences are occupied by NLI core complex members together with co-repressor ETO2 and γ-globin repressor BCL11A. The LCR and β-globin gene establish proximity in these cells. In contrast, when γ-globin transcription is re-activated by cytokines in these cells, ETO2 participation in the NLI complex at BGL3 is diminished, as is BCL11A occupancy, and both BGL3 and γ-globin are transcribed. In these cells, proximity between the BGL3/γ-globin region and the LCR is established. Thus, alternative NLI complexes mediate γ-globin transcription or silencing through long range LCR interactions involving an intergenic site of non-coding RNA transcription and ETO2 is critical to this process. ChIP-chip of GATA-1, NLI, and pol II in cell lines

2012-01-05 | GSE30047 | GEO

Distinct Ldb1/NLI complexes orchestrate γ-globin repression and re-activation through ETO2 in human adult erythroid cells.

2012-01-05 | E-GEOD-30047 | biostudies-arrayexpress

Identification of ETO2 direct target genes through integration of transcriptomic (RNAseq) and chromatin binding location (ChIPseq)

Project description:Erythroid cell lines (HEL and K562) were conditionally invalidated for the ETO2 gene using the CRISPR/Cas9 system. Gene expression profiling (RNAseq) and chromatin immunoprecipitation followed by high-throughput sequencing (ChIPseq) to assess localization of ETO2, MYB, EP300, H3K27ac and H3K4me3 was performed in control and ETO2-deficient cells. ChIPseq analyses were also performed on cells from human AEL patient-derived xenograft models.

2023-07-02 | E-MTAB-10346 | biostudies-arrayexpress

Embryonic erythropoiesis and hemoglobin switching require transcriptional repressor ETO2 to modulate chromatin accessibility and looping (RNA-Seq)

Project description:ETO2 functions as a transcription repressor and is required for the embryonic erythropoiesis and the hemoglobin switch. To gain insight into ETO2 regulatory function during human erythropoiesis, we performed RNA-seq for WT and ETO2 KO K562 cells and found that up-regulated genes upon ETO2 loss in human cells included many markers of mature erythroid cells EPB42, ALAS2, GYPA and SLC25a37. Notably, the α-globin genes (HBA1, HBA2 and HBZ) and embryonic and fetal β-globin genes (HBE1, HBG1, and HBG2) were significantly increased after deletion of ETO2. By contrast, deletion of ETO2 down-regulated the transcription factor genes (ETS1, KLF8 and SOX6) which play a negative role in globin gene expression and hemoglobin synthesis. To further explore different domain function of ETO2, we have analyzed our RNA-seq data from domain deletion cell lines compared to the cell line expressing wild type ETO2. Generally, 702 genes were found to co-regulated by three domain function of ETO2. Interestingly, the regulation of fetal globin genes, erythroid regulator (SOX5) as well as epigenetic factor (HDAC7) is required by three domain function of ETO2. During mouse embryonic erythropoiesis, our FACS-sorted and normal RNA-seq data in E14.5 fetal liver cells indicated that eto2 promoted a critical developmental transition and played an important role in globin switch from embryonic to adult β-globin transcription since its function is essential for key regulators (PU.1, BCL11A and ZBTB7A) and globin genes (Hbb-y and Hba-x) regulation.

2020-08-25 | GSE142226 | GEO

Inactivation of the nuclear interacting SET domain protein 1 (NSD1) impairs GATA1-regulated erythroid differentiation and causes erythroleukemia

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

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