Parp-2 deficiency impairs the survival of HSPCs after γ-irradiation. (A) Flow cytometry gating strategy used to analyze LSK (LT-HSC, ST-HSC, and MPP), and MP (CMP, GMP, and MEP) cells from mouse BM. (B) Representative dot-plots showing LSK (Lin^– (CD11b^–Gr1^–B220^–CD3^–Ter119^–) Sca-1⁺c-kit⁺), LT-HSC (Lin^–Sca-1⁺c-kit⁺CD135^–CD34^–), ST-HSC (Lin^–Sca-1⁺c-kit⁺CD135^–CD34⁺), MPP (Lin^–Sca-1⁺c-kit⁺CD135⁺CD34⁺), CMP (Lin^–Sca-1^–c-kit⁺CD34⁺FcγR^lo), GMP (Lin^–Sca-1^–c-kit⁺CD34⁺FcγR^hi), and MEP (Lin^–Sca-1^–c-kit⁺CD34^–FcγR^lo) population in Parp-2^−/− mice and WT littermates, both in steady-state conditions and 12 days after TBI (5 Gy). Percentage of cells in the individual subpopulations with regard to each gate is indicated in each quadrant. Values represent the mean of at least 8 mice of each genotype. (C) Graph showing the absolute number of LSK, LT-HSC, ST-HSC, MPP, CMP, GMP, and MEP cells, determined using the gating strategies shown in (A). The number of cells in each population was calculated by multiplying the percentage of each population by the total number of BM cells. Values represent the mean ± SEM of at least 8 mice of each genotype. *Statistically significant difference (P < .05). (D) Colony-forming units in the BM of WT and Parp-2^−/− mice. 4 × 10⁴ BM cells from WT and Parp-2^−/− mice, untreated (No IR) or after irradiation (IR) (2 Gy), were plated in duplicate in methylcellulose-containing media, and colonies were counted and distinguished by morphology on day 7. CFU-M, colony-forming unit-macrophage; CFU-G, colony-forming unit-granulocyte; CFU-GM, colony-forming unit-granulocyte macrophage; BFU-E, Burst-forming unit-erythroid; CFU-GEMM, colony-forming unit-granulocyte, erythroid, macrophage, megakaryocyte. Data are presented as number of colonies per 10⁶ cells. Values represent mean ± SEM from 3 independent experiments including at least 3 mice of each genotype per experiment. *Statistically significant difference (P < .05).