Mouse E11 WT and GATA2 heterozygous HSPCs
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ABSTRACT:
PROVIDER: PRJEB59592 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptome analysis from WT and Gata2 heterozygous mouse HSPCs at E11
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Project description:The transcription factor GATA2 plays a major role in the generation and maintenance of the hematopoietic system. In humans, heterozygous germline mutations in GATA2 often lead to a loss of function of one allele, causing GATA2 haploinsufficiency. In mice, Gata2 has an essential regulatory function in hematopoietic stem cell (HSC) generation and maintenance. However, whereas Gata2-null mice are lethal at embryonic day (E) 10.53, Gata2 heterozygous (Gata2+/-) mice survive to adulthood with normal blood values. However, mouse models thus emerged as a useful source to identify the function of GATA2 in HSC generation and fitness, they leave the mechanisms causing the different aspects of GATA2 deficiency syndrome largely undiscovered. Zebrafish have the advantage of having two GATA2 orthologues; Gata2a and Gata2b. Gata2a is expressed predominantly in the vasculature and is required for programming of the hemogenic endothelium. Gata2b is expressed in hematopoietic stem/progenitor cells (HSPCs) and homozygous deletion (gata2b-/-) redirects HSPCs differentiation bias, thus mimicking one of the GATA2 haploinsufficiency phenotypes found in patients. But patients carry heterozygous rather than homozygous GATA2 mutations, we specifically focused on how heterozygous Gata2b mutations could be mechanistically linked to erythro-myelodysplasia, a major clinical hallmark of GATA2 patients. To investigate the mechanisms of heterozygous GATA2 mutation caused GATA2 deficiency syndrome, we created a heterozygous gata2b mutation zebrafish model and sorted the entire progenitor and HSPC population including the lymphoid population from kidney marrow (KM) of WT and mutated zebrafish based on the scatter profile of flow cytometry for single-nucleus ATAC (snATAC) sequencing.
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Project description:GATA2 mutants were discovered in families predisposed to MDS/AML and in sporadic cases of CML-blast crisis. Promyelocytic HL-60 cells were transduced with lentiviral vectors that express GATA2 WT or T354M, 355delT or L359V mutants upon addition of 4-hydroxy tamoxifen (4HT). Microarrays were performed to identify GATA2 WT signatures and differences caused by these mutations. HL-60 cells transduced with GATA2 (WT, T354M, 355delT and L359V) lentiviruses were treated with 4HT for 24 hours and RNA isolated and gene expression measured on Affymetrix microarrays.
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Project description:To clarify the role of Gata2 in the development of Cbfb-MYH11 induced leukemia, we generated conditional Cbfb-MYH11 knockin mice with Gata2 heterozygous knockout. Leukemic cells with Gata2 heterozygous knockout gained higher number of genetic mutations and showed more aggressive phenotype in both primary and transplanted recipient mice. We compared gene expression profilings between Gata2+/+ and Gata2+/f leukemic cells with Cbfb-MYH11.
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