Jarid1b deletion compromises HSC potential. (A) Experimental design for transplantation. Five million BM cells isolated from Jarid1b^fl/flRosaCreERT2 mice were competitively transplanted (donor-to-recipient ratio of 1:1) into recipient mice, followed by exposure to tamoxifen (+TAM) or vehicle (−TAM) for 7 days to induce Jarid1b deletion from the donor BM. Primary transplant analysis of PB donor reconstitution at 4 and 22 weeks; *P = .0346, unpaired Student t test (B); PB donor lineage distribution at week 22 (C); BM donor reconstitution at week 24 (D); and frequency of LSK, MP, and CLP (Lin^–Flk2⁺IL7Rα⁺cKit^midScal^mid) populations within BM (E). Frequency of HSCs (LSKCD34⁻Flk2⁻) within the LSK compartment (F) and within the live BM (G). (H-M) Secondary transplant analysis. Using FACS, 2 million donor cells were isolated from those primary transplants showing chimerism >10% and transplanted competitively (donor-to-recipient ratio of 10:1) into secondary recipients. (H) PB donor reconstitution at 4 and 16 weeks. *P = .0205; unpaired Student t test. (I) PB donor lineage distribution at week 16. CD4/CD8: *P = .0277; Gran (granulocytes): *P = .047. (J) Representative flow cytometry plots showing donor (CD45.2) vs recipient (CD45.1) BM from mice treated with (+) or without (−) TAM. (K) BM donor reconstitution at week 17. **P = .0019; unpaired Student t test. (L) Representative flow plots of LSK gates in mice transplanted with BM treated with (+) or without (−) TAM. (M) Frequency of LSK, MP, and CLP populations within BM. MP: *P = .0104; CLP: *P = .0182; unpaired Student t test. Error bars ± standard deviation.