p53 deficiency leads to further expansion, increased quiescence, and re-plating capability of Nras^G12D/+myeloid progenitors. Control, p53^−/−, Nras^G12D/+, and Nras^G12D/+p53^−/− mice were treated with pI-pC and euthanized on day 12 for analysis as described in “Materials and methods.” (A) Quantification of MPs, CMPs, GMPs, and MEPs in BM and SP. (B) Cell cycle analysis of bone marrow GMPs and MEPs using Ki-67/4′,6-diamidino-2-phenylindole (DAPI) staining. (C) A 16-hour pulse of 5′-ethynyl-2′-deoxyuridine (EdU) to quantify proliferating bone marrow MPs. (D) 5 × 10⁴ bone marrow cells isolated from control, p53^−/−, Nras^G12D/+, or Nras^G12D/+p53^−/− mice were plated in semisolid medium without cytokines or with 0.2 ng/mL of murine GM-CSF or 10 ng/mL murine interleukin-3 (IL-3). Colonies were counted 7 to 10 days after culture. (E) Methylcellulose culture of 5 × 10⁴ bone marrow cells with 10 ng/mL murine IL-3 over 3 rounds of re-plating. Data are presented as mean ± SD. *P < .05; **P < .01; ***P < .001. n = 10∼16, a range of 10-16 mice.