Expansion of the immature megakariocytes in Npm1-TCTG/WT;Cre⁺ and Npm1-TCTG/TCTG;Cre⁺ mice. (A) Flow cytometric analysis of single-cell suspensions of BM from representative Npm1-TCTG/WT;Cre⁺, Npm1-TCTG/TCTG;Cre⁺, and Npm1-TCTG/WT;Cre⁻ pIpc-treated control mice demonstrates an increase in the percentage of Lin^–Kit⁺Sca-1^–CD150⁺CD41⁺ megakaryocytic progenitor populations. (B) Quantification of Lin^–Kit⁺Sca-1^–CD150⁺CD41⁺ MKPs in the BM of age-matched mutant mice analyzed as in panel A (n = 8 per genotype). (C) No differences in the percentage of Lin^–Kit⁺Sca-1⁺ cells and Lin^–Kit⁺Sca-1^–CD41^–CD150⁺FcgR^–CD105^lo erythromegakaryocytic progenitor cells in mutant Cre⁺ vs Cre⁻ pIpC-treated control mice (n = 6 per genotype). (D) BM cells from Npm1-TCTG/WT;Cre⁺, Npm1-TCTG/TCTG;Cre⁺, and Cre⁻ pIpC-treated mice were plated on M3434 methylcellulose medium (containing stem cell factor, IL-3, IL-6, erythropoietin) and scored for colony formation 7 to 10 days later (BFU-E, burst-forming unit-erythroid; GEMM, granulocyte, erythroid, monocyte, megakaryocyte; GM, granulocyte monocyte; M, monocyte). Results are the average of 3 independent experiments performed in duplicate (mean ± standard deviation are shown). (E) CFU-MK potential from total BM (n = 3 per genotype). (F) Photo of representative colonies (×10 magnification) from (ii) Npm1-TCTG/WT;Cre⁺ compared with (i) Npm1-TCTG/WT;Cre⁻. (G) Summary of the alterations in the development of the megakaryocytes after the expression of the NPM mutation A in the hematopoietic compartment. **P < .01; n.s. = not statistically significant.