Ki67 deficiency results in significant defects in early B cell development. (A) Total BM cell counts of WT (n = 3) and Mki67−/− (n = 3) mice. (B) Gating strategy of LK, LSK, and B-lineage cells. Representative percentages of the gated population of the parental gate are shown. (C) Quantification of cell numbers of LK, LSK, and B220+ B-lineage cells per femur in WT (n = 3) and Mki67−/− (n = 3) mice. (D) Gating strategy of B cell progenitors at pre-pro-B, pro-B, large pre-B, small pre-B, and immature B cell stage. Representative percentages of the gated populations of the parental gate are shown. (E) Quantification of cell numbers of B cell progenitors at each developmental stage per femur in WT (n = 3) and Mki67−/− (n = 3) mice. (F) Differentiation indexes calculated as the cell number of a later B cell developmental stage divided by that of the former stage in WT (n = 3) and Mki67−/− (n = 3) mice. Data in A, D, E, and F are representative of five independent experiments and in B and C are representative of two independent experiments. Statistical differences in A were determined by two-tailed unpaired t test, and in C, E, and F by multiple unpaired t tests (corrected for multiple comparisons using the Holm–Sidak method). Adjusted P values are shown. ns, P > 0.05.
Figure 2.

Ki67 deficiency results in significant defects in early B cell development. (A) Total BM cell counts of WT (n = 3) and Mki67−/− (n = 3) mice. (B) Gating strategy of LK, LSK, and B-lineage cells. Representative percentages of the gated population of the parental gate are shown. (C) Quantification of cell numbers of LK, LSK, and B220+ B-lineage cells per femur in WT (n = 3) and Mki67−/− (n = 3) mice. (D) Gating strategy of B cell progenitors at pre-pro-B, pro-B, large pre-B, small pre-B, and immature B cell stage. Representative percentages of the gated populations of the parental gate are shown. (E) Quantification of cell numbers of B cell progenitors at each developmental stage per femur in WT (n = 3) and Mki67−/− (n = 3) mice. (F) Differentiation indexes calculated as the cell number of a later B cell developmental stage divided by that of the former stage in WT (n = 3) and Mki67−/− (n = 3) mice. Data in A, D, E, and F are representative of five independent experiments and in B and C are representative of two independent experiments. Statistical differences in A were determined by two-tailed unpaired t test, and in C, E, and F by multiple unpaired t tests (corrected for multiple comparisons using the Holm–Sidak method). Adjusted P values are shown. ns, P > 0.05.

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