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Single cell RNA-seq analysis of transcriptomics in WT and E2-KO, G12D and G12D/E2-KO HSPCs from mouse bone marrow

ABSTRACT: Single cell RNA-seq analysis of transcriptomics in WT and E2-KO, G12D and G12D/E2-KO HSPCs from mouse bone marrow

PROVIDER: PRJNA655501 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12396124_1.fastq.gz	Fastqsanger.gz
	SRR12396124_2.fastq.gz	Fastqsanger.gz
	SRR12396125_1.fastq.gz	Fastqsanger.gz
	SRR12396125_2.fastq.gz	Fastqsanger.gz
	SRR12396126_1.fastq.gz	Fastqsanger.gz

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Single cell RNA-seq analysis of transcriptomics in WT and E2-KO, G12D and G12D/E2-KO HSPCs from mouse bone marrow

Project description:Cancers develop from the accumulation of somatic mutations, yet it remains unclear how oncogenic lesions cooperate to drive cancer progression. Using a mouse model harboring NRasG12D and EZH2 mutations that recapitulates leukemic progression, we employ single-cell RNA sequencing to map cellular composition and gene expression alterations in healthy or diseased bone marrows underlying leukemia progression. At cellular levels, while NRasG12D induces myeloid-biased differentiation and EZH2-deficiency impairs myeloid maturation, they cooperate to promote myeloid expansion with dysregulated transcriptional programs. At gene levels, NRasG12D and EZH2-deficiency independently or synergistically control gene expression in single cells. We integrate results from histopathology, flow cytometry, leukemia repopulation, and leukemia-initiating cell assays to validate transcriptome-based cellular profiles. We use this resource to relate developmental hierarchies to leukemia phenotypes, evaluate oncogenic cooperation at single-cell levels, and identify new regulators of leukemia-initiating cells. Our studies establish an integrative approach to capture the kinetics of cancer evolution in vivo.

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