Loss of 1 allele of c-Myc impairs HSC repopulation capacity. (A-B) Flow cytometric analysis of donor-derived CD45.2⁺CD45.1⁻ cells and WT competitor–derived CD45.1⁺ CD45.2⁺ cells in recipient WT mice. (A) The ratio of donor-derived to WT competitor–derived cells in PB in recipient mice 1 to 6 months after transplantation; (B) representative plots after transplantation. (C) Flow cytometric analysis of the ratio of donor-derived to WT competitor–derived myeloid cells, B cells, and T cells in PB in recipient mice 6 months after transplantation. (D) Flow cytometric analysis of the ratio of donor-derived to WT competitor-derived cell populations in BM in recipient mice 6 months after transplantation (n = 5). (E-F) Total number of HPCs (E) and HSCs (F) in WT and c-Myc HET–recipient mice at 4 months after induction of c-Myc deletion. (G) Flow cytometric analysis of cell cycle status in WT and c-Myc HET LT-HSCs in recipient mice, as determined by a BrdU incorporation assay (n = 5). (H) Flow cytometric analysis of cell cycle status in WT and c-Myc HET LT-HSCs in recipient mice. Cells were stained with Hoechst DNA dye and pyroninY RNA dye (n = 5). (I) Flow cytometric analysis of the ratio of donor-derived to WT competitor-derived cells in the recipient mice; (J) representative plots are shown 1 and 5 months after transplantation. pIpC was injected 1 month after transplantation. (K) Flow cytometric analysis of the ratio of donor-derived to WT competitor–derived myeloid cells and, B and T cells in PB in the recipient mice 5 months after transplantation (n = 5). *P < .05; **P < .01; ***P < .001, by Student t test.