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Human erythroleukemia genetics and transcriptomes identify master transcription factors as functional disease drivers

ABSTRACT: Human erythroleukemia genetics and transcriptomes identify master transcription factors as functional disease drivers

PROVIDER: PRJEB38084 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4082990_1.fastq.gz	Fastqsanger.gz
	ERR4082990_2.fastq.gz	Fastqsanger.gz
	ERR4082984_1.fastq.gz	Fastqsanger.gz
	ERR4082984_2.fastq.gz	Fastqsanger.gz
	ERR4082985_1.fastq.gz	Fastqsanger.gz

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Human erythroleukemia genetics and transcriptomes identify master transcription factors as functional disease drivers

Project description:We have identified aberrant expression ok key master transcription factor in an AEL patient cohort. The ectopic expression of these factors in mouse erythroid progenitors lead to their transformation in vitro. Then we investigated chromatin accessibility by ATACseq in these models and compared them to normal erythroid progenitors.

2020-06-01 | E-MTAB-9012 | biostudies-arrayexpress

Human erythroleukemia genetics and transcriptomes identify master transcription factors as functional disease drivers.

Project description:Acute erythroleukemia (AEL or acute myeloid leukemia [AML]-M6) is a rare but aggressive hematologic malignancy. Previous studies showed that AEL leukemic cells often carry complex karyotypes and mutations in known AML-associated oncogenes. To better define the underlying molecular mechanisms driving the erythroid phenotype, we studied a series of 33 AEL samples representing 3 genetic AEL subgroups including TP53-mutated, epigenetic regulator-mutated (eg, DNMT3A, TET2, or IDH2), and undefined cases with low mutational burden. We established an erythroid vs myeloid transcriptome-based space in which, independently of the molecular subgroup, the majority of the AEL samples exhibited a unique mapping different from both non-M6 AML and myelodysplastic syndrome samples. Notably, >25% of AEL patients, including in the genetically undefined subgroup, showed aberrant expression of key transcriptional regulators, including SKI, ERG, and ETO2. Ectopic expression of these factors in murine erythroid progenitors blocked in vitro erythroid differentiation and led to immortalization associated with decreased chromatin accessibility at GATA1-binding sites and functional interference with GATA1 activity. In vivo models showed development of lethal erythroid, mixed erythroid/myeloid, or other malignancies depending on the cell population in which AEL-associated alterations were expressed. Collectively, our data indicate that AEL is a molecularly heterogeneous disease with an erythroid identity that results in part from the aberrant activity of key erythroid transcription factors in hematopoietic stem or progenitor cells.

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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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