Mutations in Ifngr1 and Stat1 rescue phenotypic and functional defects in Irgm1-deficient HSCs. (A) Gene expression of Ccnb1 and Ccl5 in HSCs (CD150⁺ SP^KLS) from WT, Irgm1^−/−, Ifngr1^−/−, Irgm1^−/−Ifngr1^−/−, Stat1^−/−, and Irgm1^−/−Stat1^−/− was analyzed by the use of quantitative RT-PCR. Bars represent n = 3. (B) Noncompetitive BM transplants were performed by the use of WBM from CD45.2 WT, Irgm1^−/−, Irgm1^−/−Ifngr1^−/−, or Irgm1^−/−Stat1^−/− donors at a dose of 2 × 10⁶ cells. Engraftment was monitored by flow cytometric analysis of peripheral blood chimerism at the indicated time points. n = 3-5 for each bar. (C) HSC proliferation status was assessed by in vivo BrdU labeling. CD150⁺ SP^KLS cells were purified from mice after 3 days of exposure to BrdU. The percentage of CD150⁺ SP^KLS cells that incorporated BrdU during the labeling period is indicated. Bars indicate the mean and SEM and are representative of 2 independent experiments, each performed in triplicate. *P < .05, **P < .01, ***P < .001.