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

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

PROVIDER: PRJNA844979 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19526528_1.fastq.gz	Fastqsanger.gz
	SRR19526528_2.fastq.gz	Fastqsanger.gz
	SRR19526529_1.fastq.gz	Fastqsanger.gz
	SRR19526529_2.fastq.gz	Fastqsanger.gz
	SRR19526530_1.fastq.gz	Fastqsanger.gz

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

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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

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

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 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)

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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)

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

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

| PRJNA845216 | ENA

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

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

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

Project description:The NFIA-ETO2 fusion blocks terminal erythroid maturation and induces pure erythroid leukemia in cooperation with mutant TP53

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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 blocks terminal erythroid maturation and induces pure erythroid leukemia (PEL) in cooperation with mutant TP53

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Control of developmentally primed erythroid genes by combinatorial corepressor actions

Project description:How transcription factors (TFs) cooperate within large protein complexes to allow rapid modulation of gene expression during development is still largely unknown. Here we show that the key haematopoietic LIM-domain-binding protein-1 (LDB1) TF complex contains several activator and repressor components that together maintain an erythroid-specific gene expression programme primed for rapid activation until differentiation is induced. A combination of proteomics, functional genomics and in vivo studies presented here identifies known and novel co-repressors, most notably the ETO2 and IRF2BP2 proteins, involved in maintaining this primed state. The ETO2â??IRF2BP2 axis, interacting with the NCOR1/SMRT co-repressor complex, suppresses the expression of the vast majority of archetypical erythroid genes and pathways until its decommissioning at the onset of terminal erythroid differentiation. Our experiments demonstrate that multimeric regulatory complexes feature a dynamic interplay between activating and repressing components that determines lineage-specific gene expression and cellular differentiation. ChIP-Sequencing profiles of the IRF2BP2, GFI1B and LSD1 proteins were generated using mouse erythroleukemia (MEL) cells. RNA-seq experiments of Irf2bp2-WT, Irf2bp2-KD, Eto2-WT, Eto2-KD, Gfi1b-WT, Gfi1b-KD, Lsd1-WT, Lsd1-KD, MEL-non-induced, and MEL-induced stages were performed using standard RNA-seq protocol. Illumina HiSeq 2000 (standard TruSeq RNA sequencing protocol) was used for the sequencing.

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