Figure 4.
Figure 4. Zeb2 deletion causes impaired differentiation at different stages of maturation. (A) Representative FACS plots demonstrating B lymphopoiesis in control and Zeb2Δ/ΔMx1-Cre BM cells gated on B220-positive population. (B) Frequency calculation of B-cell progenitors within the B220-positive BM subpopulation in 3 repetitive analyses revealed a block at the transition from prepro-B to pro-B cell stage. Data from 3 independent biological replicates are shown as means ± SEM. **P < .01; ***P < .001. (C) Representative FACS plots showing megakaryocytic progenitors in control and Zeb2Δ/ΔMx1-Cre BM cells gated on Lin−cKit+Sca1−CD16/32− population. (D) Analyses of megakaryocytic and erythroid progenitors within total BM cells in 3 repetitive analyses revealed an increase of MkP, PreMegE, and pre CFU-E cells in Zeb2-deficient mice compared with controls. Data from 6 independent biological replicates are shown as means ± SEM. **P < .01; ***P < .001. (E) Representative images of BM sections from femurs from Zeb2Δ/ΔMx1-Cre and control mice showing abnormal morphology in Zeb2-deficient megakaryocytes (arrow) compared with controls. Bar graphs, 50 µm. (F) Representative images of acetylcholinesterase staining of CFU-megakaryocyte colonies demonstrate the absence of mature megakaryocytes in cell cultures derived from Zeb2Δ/ΔMx1-Cre mice.

Zeb2 deletion causes impaired differentiation at different stages of maturation. (A) Representative FACS plots demonstrating B lymphopoiesis in control and Zeb2Δ/ΔMx1-Cre BM cells gated on B220-positive population. (B) Frequency calculation of B-cell progenitors within the B220-positive BM subpopulation in 3 repetitive analyses revealed a block at the transition from prepro-B to pro-B cell stage. Data from 3 independent biological replicates are shown as means ± SEM. **P < .01; ***P < .001. (C) Representative FACS plots showing megakaryocytic progenitors in control and Zeb2Δ/ΔMx1-Cre BM cells gated on LincKit+Sca1CD16/32 population. (D) Analyses of megakaryocytic and erythroid progenitors within total BM cells in 3 repetitive analyses revealed an increase of MkP, PreMegE, and pre CFU-E cells in Zeb2-deficient mice compared with controls. Data from 6 independent biological replicates are shown as means ± SEM. **P < .01; ***P < .001. (E) Representative images of BM sections from femurs from Zeb2Δ/ΔMx1-Cre and control mice showing abnormal morphology in Zeb2-deficient megakaryocytes (arrow) compared with controls. Bar graphs, 50 µm. (F) Representative images of acetylcholinesterase staining of CFU-megakaryocyte colonies demonstrate the absence of mature megakaryocytes in cell cultures derived from Zeb2Δ/ΔMx1-Cre mice.

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