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MRNA profiles of CD43++c-kit+, CD43+c-kit- and CD43-c-Kit- AML1-ETO9a murine leukemic bone marrow cells

ABSTRACT: mRNA profiles of CD43++c-kit+, CD43+c-kit- and CD43-c-Kit- AML1-ETO9a murine leukemic bone marrow cells

PROVIDER: PRJNA772178 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16464717_1.fastq.gz	Fastqsanger.gz
	SRR16464717_2.fastq.gz	Fastqsanger.gz
	SRR16464718_1.fastq.gz	Fastqsanger.gz
	SRR16464718_2.fastq.gz	Fastqsanger.gz
	SRR16464719_1.fastq.gz	Fastqsanger.gz

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mRNA profiles of CD43++c-kit+, CD43+c-kit- and CD43-c-Kit- AML1-ETO9a murine leukemic bone marrow cells

Project description:We discovered a spontaneous differentiation path characterized by CD43 and c-Kit in the AE9a murine model, where the leukemia-initiating potential is lost while leukemic cells display features of erythroid maturation. Therefore, we sorted out CD43++c-Kit+, CD43+c-Kit- and CD43-c-Kit- AE9a leukemic cells for RNA-sequencing analyses to determine the underlying transcriptome.

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Project description:T(8;21), which produces the AML1-ETO (AE) fusion oncoprotein, is one of the most common chromosomal abnormalities in AML patients. Despite its prevalence among patients, it has remained challenging to study the impact of AE on leukemia development in vivo due to limitations of the current t(8;21) mouse models. Here, we devised a germline transmitted transgenic Rosa26-AE9a knock-in mouse model that expresses AE9a protein, a truncated AE variant, at moderately elevated levels compared to endogenous RUNX1. These mice develop myeloid leukemia with longer latency and lower penetrance compared to mice using the AE9a retroviral transduction-transplantation model. Pre-leukemic mice exhibited myeloid progenitor skewing in their bone marrow, with more granulocyte-monocyte progenitors (GMP) at the expense of megakaryocyte-erythroid progenitors (MEP). Importantly, hematopoietic stem and progenitor cells (HSPCs) of pre-leukemic mice had increased clonogenic potential. We performed single cell RNA-sequencing on pre-leukemic HSPCs and confirmed both this granulocytic bias and hindered differentiation. Overall, we have overcome the limitation of uncontrolled AE9a oncogene expression in the retroviral transduction-transplantation mouse model and have devised a new germline transmitted Rosa26 locus AE9a knock-in model that more faithfully represents t(8;21) human disease.

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