![Coexistence of the Srsf2 P95H mutation and Runx1 deficiency leads to MDS phenotypes in vivo. (A) Schematic diagram of the noncompetitive BMT experiments. (B) Total amount of hemoglobin (Hb), number of red blood cells (RBCs), and mean corpuscular volume (MCV) in the peripheral blood of recipient mice at 16 weeks after BMT (wild-type [WT], n = 19; Srsf2P95H/+, n = 23; Runx1 knockout, n = 24; double mutant, n = 27); time course analysis of Hb. (C) Total number of platelets (PLTs) in the peripheral blood of recipient mice at 16 weeks after BMT (WT, n = 19; Srsf2P95H/+, n = 23; Runx1 knockout, n = 24; double mutant, n = 27); time course analysis of platelet. (D) Total number of white blood cells (WBCs) in the peripheral blood of recipient mice at 16 weeks after BMT (WT, n = 19; Srsf2P95H/+, n = 23; Runx1 knockout, n = 24; double mutant, n = 27); time course analysis of WBC. (E) Peripheral blood smears of recipient mice. Dysplastic cells are indicated and include hyper/hyposegmented neutrophils (insets) and Howell-Jolly bodies (nuclear remnants) in RBCs (arrows). Smears are representative of 3 mice per genotype. The frequencies of dysplastic erythroid cells and neutrophils in each genotype are indicated in the graphs to the right. Absolute numbers of myeloid cells (Cd11b+) (F) and B cells (B220+) (G) in the peripheral blood of mice at the indicated times after BMT. Data are mean ± standard error of the mean (SEM). Significance was determined by 1-way analysis of variance (ANOVA) with Tukey post hoc test. ∗P < .05, ∗∗P < .01.](https://ash.silverchair-cdn.com/ash/content_public/journal/bloodadvances/6/23/10.1182_bloodadvances.2022007804/4/blooda_adv-2022-007804-gr1.jpeg?Expires=1735844101&Signature=gnGjGESGSavlLSGnd~iQA8sHfGGCnzboNL2JEBDCMepJ6C~1bU6cCFkM4B6FQxNV2L32Aw7INcF~gO-XjF~T1syYYzbRmlRm9p0RTbMZSXtWmBNyg-79RQiI-AT-zf8BkSSstZeio3DIcO15p-jrD9i1jyAhwGqZgomn0n26e4yO5Arxasszr6qIltDfbmKlxq~EQ3ex4ImPbMoAhej2bZxdVk-hmHjmmdpaXhtQUryd6ZDJVHudVKZSf00A40gHA9M8zjCN4Kqct-k9qLNmyCYnsvhwEfAAEqL0VFJgDj9EY4rhDdgmyPvAPQ9sHH-f3z2keiRev5SmxRU9h81ZCg__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
Coexistence of the Srsf2 P95H mutation and Runx1 deficiency leads to MDS phenotypes in vivo. (A) Schematic diagram of the noncompetitive BMT experiments. (B) Total amount of hemoglobin (Hb), number of red blood cells (RBCs), and mean corpuscular volume (MCV) in the peripheral blood of recipient mice at 16 weeks after BMT (wild-type [WT], n = 19; Srsf2P95H/+, n = 23; Runx1 knockout, n = 24; double mutant, n = 27); time course analysis of Hb. (C) Total number of platelets (PLTs) in the peripheral blood of recipient mice at 16 weeks after BMT (WT, n = 19; Srsf2P95H/+, n = 23; Runx1 knockout, n = 24; double mutant, n = 27); time course analysis of platelet. (D) Total number of white blood cells (WBCs) in the peripheral blood of recipient mice at 16 weeks after BMT (WT, n = 19; Srsf2P95H/+, n = 23; Runx1 knockout, n = 24; double mutant, n = 27); time course analysis of WBC. (E) Peripheral blood smears of recipient mice. Dysplastic cells are indicated and include hyper/hyposegmented neutrophils (insets) and Howell-Jolly bodies (nuclear remnants) in RBCs (arrows). Smears are representative of 3 mice per genotype. The frequencies of dysplastic erythroid cells and neutrophils in each genotype are indicated in the graphs to the right. Absolute numbers of myeloid cells (Cd11b+) (F) and B cells (B220+) (G) in the peripheral blood of mice at the indicated times after BMT. Data are mean ± standard error of the mean (SEM). Significance was determined by 1-way analysis of variance (ANOVA) with Tukey post hoc test. ∗P < .05, ∗∗P < .01.
