Chromation accessibility profiles of cKit positive bone marrow cells from six genotype mice - WT, Idh1R132, Npm1c, Flt3ITD, Idh1R132+Npm1c, and Idh1R132+Flt3ITD

Here we show that the combination of Idh1R132 plus Npm1c mutations cooperatively induced overt AML in vivo, using genetically engineered mouse model. In contrast, the combination of Idh1R132 plus Flt3ITD led to myeloid proliferation disease, but not AML. The mice harboring both of Idh1R132 and Npm1c mutations got fatal (median survival, 254 days) due to AML, which demonstrated rapid lethality on recipient mice in secondary transplantation experiments. We analyzed cKit-positive bone marrow cells from six genotype mice - WT, Idh1R132, Npm1c, Flt3ITD, Idh1R132+Npm1c, and Idh1R132+Flt3ITD. We isolated cKit positive BM cells from the mice of the two different ages (3 and 6 months old), and subjected to RNA-seq, bisulfite-seq, and ATAC-seq. We examined gene-wide chromatin accessibility profiles of cKit positive BM cells from six genotype mice - WT, Idh1R132, Npm1c, Flt3ITD, Idh1R132+Npm1c, and Idh1R132+Flt3ITD, with 3-4 biological replicates for each genotype. We examined the cells from mice of the two different ages (3 and 6 months old).