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Loss of Dnmt3a Immortalizes Hematopoietic Stem Cells in vivo

ABSTRACT: Loss of Dnmt3a Immortalizes Hematopoietic Stem Cells in vivo

PROVIDER: PRJNA384231 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5481093_1.fastq.gz	Fastqsanger.gz
	SRR5481093_2.fastq.gz	Fastqsanger.gz
	SRR5481094_1.fastq.gz	Fastqsanger.gz
	SRR5481094_2.fastq.gz	Fastqsanger.gz
	SRR5481095_1.fastq.gz	Fastqsanger.gz

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Loss of Dnmt3a Immortalizes Hematopoietic Stem Cells in vivo [WGBS]

Project description:Recent epidemiological studies have shown that cancer-associated DNMT3A mutations can be detected in the blood of a large proportion of asymptotic elderly individuals. It is important to understand how these mutations provide a competitive advantage to HSCs and allow them to establish clonal dominance. Here we demonstrate that the stress of serial HSC transplantation immortalizes Dnmt3a-null HSCs.

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Loss of Dnmt3a Immortalizes Hematopoietic Stem Cells In Vivo.

Project description:Somatic mutations in DNMT3A are recurrent events across a range of blood cancers. Dnmt3a loss of function in hematopoietic stem cells (HSCs) skews divisions toward self-renewal at the expense of differentiation. Moreover, DNMT3A mutations can be detected in the blood of aging individuals, indicating that mutant cells outcompete normal HSCs over time. It is important to understand how these mutations provide a competitive advantage to HSCs. Here we show that Dnmt3a-null HSCs can regenerate over at least 12 transplant generations in mice, far exceeding the lifespan of normal HSCs. Molecular characterization reveals that this in vivo immortalization is associated with gradual and focal losses of DNA methylation at key regulatory regions associated with self-renewal genes, producing a highly stereotypical HSC phenotype in which epigenetic features are further buttressed. These findings lend insight into the preponderance of DNMT3A mutations in clonal hematopoiesis and the persistence of mutant clones after chemotherapy.

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Dnmt3a regulates myeloproliferation and liver-specific homing and expansion of hematopoietic stem and progenitor cells (Bisulfite-Seq)

Project description:DNMT3A mutations are observed in myeloid malignancies, including myeloproliferative neoplasms (MPN), myelodysplastic syndromes (MDS), and acute myeloid leukemia (AML). Here we investigated the impact of conditional hematopoietic Dnmt3a loss on disease phenotype in primary mice. Dnmt3a ablation led to a lethal, fully penetrant myeloproliferative neoplasm with myelodysplasia (MDS/MPN) characterized by marked, progressive hepatomegaly that was transplantable. We detected expanded stem/progenitor populations in the liver of Dnmt3a-ablated mice. Homing studies showed that Dnmt3a-deleted bone marrow cells preferentially migrated to the liver. Hence, in addition to the established role of Dnmt3a in regulating self-renewal, Dnmt3a regulates tissue tropism and limits myeloid progenitor expansion in vivo.

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