Parp-2 deficiency affects BM-repopulating capacity of HSCs after expansion stress. (A) Flow cytometric analysis of peripheral blood cells isolated from either Parp-2^−/− (n = 5) or WT (n = 5) recipient mice (CD45.2⁺) at 6 and 12 weeks after TBI (5 Gy) and the injection of WT congenic CD45.1⁺ BM cells. Cells were stained with anti-CD45.1 and anti-CD45.2 mAb. Percentages of cells in the individual subpopulations are indicated in each quadrant. (B) Scheme detailing competitive BM reconstitution using total BM cells from irradiated (5 Gy or 2 Gy) (left) and nonirradiated (right) WT or Parp-2^−/− donor mice expressing the CD45.2 leukocyte cell surface marker in fixed ratios with WT B6.SJL competitor BM cells expressing CD45.1 and transplanted into lethally irradiated (9 Gy) B6 x B6.SJL F1 (CD45.1/CD45.2) recipient mice. (C) Graph showing the percentage of donor-derived (CD45.2) cells in the peripheral blood of B6 × B6.SJL F1 (CD45.1/CD45.2) recipients at 12 weeks after transplantation. Values represent the mean ± SEM of at least 6 mice of each genotype. *Statistically significant difference (P < .05). (D) Results of secondary transplants in which each secondary recipient received 2 × 10⁶ BM cells from a primary recipient 16 weeks after the primary transplantation. The graph shows the percentage of donor-derived CD45.2⁺ cells in the peripheral blood of B6 × B6.SJL F1 (CD45.1/CD45.2) recipients at 12 weeks after transplantation. Values represent the mean ± SEM of at least 6 mice of each group. *Statistically significant difference (P < .05).