Twist1 deletion compromises reconstitution and self-renewal capacity of HSCs. (A) Schematic for competitive and secondary BM transplantations. (B) Percentage of donor-derived CD45.2 chimerism in the PB of primary recipients. Excision occurred 3 weeks before transplantation (n = 5-10). (C) Chimerism of donor-derived BM cells at 20 weeks after primary BM transplantation (BMT; n = 5). (D-E) Frequencies and absolute numbers of donor-derived indicated populations in CD45.2⁺ BM at 20 weeks after primary BMT (n = 5). (F) Homing assay was performed by transplantation of 5000 LT-HSCs from control (Ctrl) or cKO mice into lethally irradiated wild-type (WT) mice. Absolutes number of CD45.2⁺ cells homing to recipient BM are shown (n = 5). (G) Schematic for competitive BMTs. (H) Percentage of CD45.2 chimerism in the PB of primary recipients after gene deletion in recipient mice (n = 4-6). (I) Chimerism of donor-derived PB cells after secondary BMT (n = 4-6). CD45.2⁺ LT-HSCs from primary BMT mice were transplanted into lethally irradiated secondary recipients. (J) Schematic for reciprocal BMTs. (K) Chimerism of CD45.1⁺ cells in PB of cKO and Ctrl recipients at the indicated time points after BMT (n = 8-9). Data are shown as means ± standard deviation. *P < .05, **P < .01, ***P < .001 (Student t test). ns, not significant; pI:pC, polyinosinic:polycytidilic acid.