Abrogation of p53-dependent apoptotic function partially rescues the proliferative defects observed in Pot1b^Δ/Δ;mTerc^+/− HSCs. (A) Frequency of LK and LSK cells isolated from age-matched wild-type, p53^P/P, Pot1b^Δ/Δ; mTerc^+/−, and Pot1b^Δ/Δ; mTerc^+/−; p53^P/P BM. (B) BM morphology of age-matched wild-type (WT) p53^P/P, Pot1b^Δ/Δ; mTerc^+/−, and Pot1b^Δ/Δ; mTerc^+/−; p53^P/P mice (×20 magnification) in the diaphysis of the bone. (C) Representative in vitro colony-forming assays of 10⁴ BM mononucleated cells isolated from age-matched wild-type, p53^P/P, Pot1b^Δ/Δ; mTerc^+/−;p53^P/P, and Pot1b^Δ/Δ; mTerc^+/− mice. (D) Quantification of the number of colonies shown in panel C. The average colony numbers for wild-type (WT) p53^P/P, Pot1b^Δ/Δ; mTerc^+/−, and Pot1b^Δ/Δ; mTerc^+/−; p53^P/P mice are 73 ± 12, 84 ± 15, 9 ± 5, and 35 ± 8, respectively. Results are from 3 independent experiments. Error bars represent SEM. (E) Kaplan-Meier survival analysis of Pot1b^Δ/Δ; mTerc^+/−; p53^P/P intercrosses and wild-type (WT), p53^P/P mice as control. For clarity, not all genotypes generated are shown. P values are indicated for selected comparison groups.