Figure 6
Figure 6. Lack of HMGA2 rescues myeloid progenitor expansion caused by loss of RUNX1. Percentages of hematopoietic stem cell populations analyzed by flow cytometry, including (A) GMPs, (B) CMPs, and (C) MEPs. For myeloid progenitor staining, mice used were: wild-type (Hmga2+/+ or Hmga2+/−, Runx1(fl/fl), Mx1Cre–, n = 9), Hmga2−/− (Hmga2−/−, Runx1(fl/fl), Mx1Cre–, n = 9), Runx1Δ/Δ (Hmga2+/+ or Hmga2+/−, Runx1(fl/fl), Mx1Cre+, n = 14), and Double KO (Hmga2−/−, Runx1(fl/fl), Mx1Cre+, n = 8). (D) Representative flow cytometry gating of GMP, CMP, and MEP populations on each of the 4 genotypes of mice and their averages are shown. (E-G) Averages of frequencies of Annexin V–positive/7AAD-negative cells from the (E) GMP, (F) CMP, and (G) MEP gates of each genotype (n = 4 each) are shown. *P < .05.

Lack of HMGA2 rescues myeloid progenitor expansion caused by loss of RUNX1. Percentages of hematopoietic stem cell populations analyzed by flow cytometry, including (A) GMPs, (B) CMPs, and (C) MEPs. For myeloid progenitor staining, mice used were: wild-type (Hmga2+/+ or Hmga2+/−, Runx1(fl/fl), Mx1Cre, n = 9), Hmga2−/− (Hmga2−/−, Runx1(fl/fl), Mx1Cre, n = 9), Runx1Δ/Δ (Hmga2+/+ or Hmga2+/−, Runx1(fl/fl), Mx1Cre+, n = 14), and Double KO (Hmga2−/−, Runx1(fl/fl), Mx1Cre+, n = 8). (D) Representative flow cytometry gating of GMP, CMP, and MEP populations on each of the 4 genotypes of mice and their averages are shown. (E-G) Averages of frequencies of Annexin V–positive/7AAD-negative cells from the (E) GMP, (F) CMP, and (G) MEP gates of each genotype (n = 4 each) are shown. *P < .05.

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