Figure 3.
Chd7 deficiency inhibits proliferation of Lin–and LK populations in Cbfb-MYH11 mice. (A-D) The indicated groups of mice were treated with ENU to induce additional mutations and with poly(I:C) to induce the expression of Cbfb-MYH11 and/or Chd7 deficiency. Three weeks after poly(I:C) treatment, mice were euthanized after being treated with BrdU for 1 hour, and a BrdU incorporation assay was performed. (A-B) Representative FACS plots of cells stained for 7-aminoactinomycin D (7-AAD) and BrdU that were gated on (A) Lin– population and (B) LK population. (C-D) The percentages of BrdU+ cells in (C) Lin– or (D) LK cell population are shown (mean ± SEM). Three mice each for control and the Chd7f/fMx1-Cre groups and 6 mice each for Mx1-CreCbfb+/56M and Chd7f/fMx1-CreCbfb+/56M groups were used in the experiments. *P < .05.

Chd7 deficiency inhibits proliferation of Lin–and LK populations in Cbfb-MYH11 mice. (A-D) The indicated groups of mice were treated with ENU to induce additional mutations and with poly(I:C) to induce the expression of Cbfb-MYH11 and/or Chd7 deficiency. Three weeks after poly(I:C) treatment, mice were euthanized after being treated with BrdU for 1 hour, and a BrdU incorporation assay was performed. (A-B) Representative FACS plots of cells stained for 7-aminoactinomycin D (7-AAD) and BrdU that were gated on (A) Lin– population and (B) LK population. (C-D) The percentages of BrdU+ cells in (C) Lin– or (D) LK cell population are shown (mean ± SEM). Three mice each for control and the Chd7f/fMx1-Cre groups and 6 mice each for Mx1-CreCbfb+/56M and Chd7f/fMx1-CreCbfb+/56M groups were used in the experiments. *P < .05.

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