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Mus musculus Gata2 +9.5 Ets C>T transition untreated and 10 days post 5-FU LSK cells

ABSTRACT: Mus musculus Gata2 +9.5 Ets C>T transition untreated and 10 days post 5-FU LSK cells

PROVIDER: PRJNA507449 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8258120.fastq.gz	Fastqsanger.gz
	SRR8258140.fastq.gz	Fastqsanger.gz
	SRR8258111.fastq.gz	Fastqsanger.gz
	SRR8258121.fastq.gz	Fastqsanger.gz
	SRR8258131.fastq.gz	Fastqsanger.gz

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Mus musculus Gata2 +9.5 Ets C>T transition untreated and 10 days post 5-FU LSK cells

Project description:The development and function of stem and progenitor cells that produce blood cells are vital in physiology. GATA2 mutations cause immunodeficiency, myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). GATA-2 physiological activities necessitate that it be strictly regulated and cell type-specific enhancers fulfill this role. The +9.5 intronic enhancer harbors multiple conserved cis-elements, and germline mutations of these cis-elements are pathogenic in humans. Since mechanisms underlying how GATA2 enhancer disease mutations impact hematopoiesis and pathology are unclear, we generated mouse models of the enhancer mutations. While a multi-motif mutant was embryonic lethal, a single-nucleotide Ets motif mutant was viable and steady-state hematopoiesis was normal. However, the Ets motif mutation abrogated stem/progenitor cell regeneration following stress. These results reveal a new mechanism in human genetics in which a disease mutation inactivates enhancer regenerative activity, while sparing developmental activity. Mutational sensitization to stress that instigates hematopoietic failure constitutes a paradigm for GATA-2-dependent pathogenesis.

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