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. 2022 Oct 10;6(23):6078–6092. doi: 10.1182/bloodadvances.2022007804

Figure 3.

Figure 3.

Runx1 loss exacerbates the competitive disadvantage of Srsf2 P95H HSPCs. (A) Schematic diagram of the competitive BMT experiments. (B) Percentage of CD45.2+ cells, as measured by flow cytometry, in the peripheral blood of mice at the indicated time following competitive BMT (WT, n = 6; Srsf2P95H/+, n = 8; Runx1 knockout, n = 7; double mutant, n = 7). (C) Percentages of T cells (CD3+), myeloid cells (CD11b+), and B cells (B220+) in CD45.2+ peripheral blood cells of mice 24 weeks after transplantation (WT, n = 6; Srsf2P95H/+, n = 8; Runx1 knockout, n = 7; double mutant, n = 7). (D) CD45.2 chimerism of all cells in the peripheral blood, spleen, and BM of mice at 24 weeks after transplantation (WT, n = 6; Srsf2P95H/+, n = 8; Runx1 knockout, n = 7; double mutant, n = 7). (E) CD45.2 chimerism of each stem and progenitor cell compartment in the BM of mice 24 weeks after transplantation (WT, n = 6; Srsf2P95H/+, n = 8; Runx1 knockout, n = 7; double mutant, n = 7). The surface markers indicative of each progenitor population are listed in Figure 2A-D. Data are mean ± SEM. Significance was determined by 1-way ANOVA with Tukey post hoc test. ∗P < .05, ∗∗P < .01.