Platelet production proceeds normally in the absence ofcaspase-9. (A) BM megakaryocyte number is not altered in caspase-9–deficient FLC-reconstituted mice. Average number of megakaryocytes in histologic sections of BM per 10 high-powered fields of view (FOV; original magnification, ×200). Data represent mean ± SD; n = 10-12 mice per genotype. (B) Spleen megakaryocyte number is not altered in Casp9^−/− FLC-reconstituted mice. Average number of megakaryocytes in histologic sections of spleen per 5 high-powered FOV (original magnification, ×600). Data represent mean ± SD; n = 4-6 mice per genotype. (C) The megakaryocyte ploidy distribution profile of CD41⁺ BM cells is moderately altered by caspase-9 deficiency. Data represent mean ± SD; n = 4-8 mice per genotype; **P < .01. (D) Casp9^−/− FLC-reconstituted mice have serum TPO levels equivalent to wild type. Data represent mean ± SEM; n > 10 mice per genotype. (E) Loss of caspase-9 does not perturb proplatelet formation. FLC-derived megakaryocytes were visually scored for proplatelet formation over the time indicated. Data represent the mean ± SD; n = 4-5 fetal livers per genotype. (F) Representative microscopic image of Casp9^+/+ and Casp9^−/− FLC-derived mature megakaryocytes forming proplatelets in culture. Original magnification, ×400.