Figure 4
Figure 4. HSC defects in Dot1l-deficient cells are cell-autonomous. CD45.2+ Dot1lwt/wt;CreER+ (Dot1l+/+) or Dot1lF/F;CreER+ (Dot1lF/F) cells and CD45.1+ competitors were mixed at 1:1 ratio and transplanted into lethally irradiated (900 cGy) CD45.1+ congenic recipients. (A) Once bone marrow was reconstituted 8 weeks after transplantation, recipients were injected with tamoxifen. Blood was collected from recipients on indicated weeks after tamoxifen injection and stained for 3 lineages. After the Dot1l excision, Dot1lF/F cells rapidly disappeared from peripheral blood. Data are mean ± SD. (B) Bar graph of bone marrow and thymus reconstitution by CD45.2+ cells 16 weeks after tamoxifen injection. Dot1lF/F cells minimally remained in the recipients. Data are mean ± SD.

HSC defects in Dot1l-deficient cells are cell-autonomous. CD45.2+Dot1lwt/wt;CreER+ (Dot1l+/+) or Dot1lF/F;CreER+ (Dot1lF/F) cells and CD45.1+ competitors were mixed at 1:1 ratio and transplanted into lethally irradiated (900 cGy) CD45.1+ congenic recipients. (A) Once bone marrow was reconstituted 8 weeks after transplantation, recipients were injected with tamoxifen. Blood was collected from recipients on indicated weeks after tamoxifen injection and stained for 3 lineages. After the Dot1l excision, Dot1lF/F cells rapidly disappeared from peripheral blood. Data are mean ± SD. (B) Bar graph of bone marrow and thymus reconstitution by CD45.2+ cells 16 weeks after tamoxifen injection. Dot1lF/F cells minimally remained in the recipients. Data are mean ± SD.

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