Loss ofcaspase-9 modifies the kinetics of ABT-737–induced thrombocytopenia but not platelet lifespan at steadystate. (A) Steady-state platelet clearance can proceed independently of caspase-9. Survival of in vivo biotinylated platelets was determined by pulse-chase experiments. After whole-blood labeling with biotin, blood samples were obtained by tail bleeding at time intervals and the disappearance of circulating platelets. Data represent the mean ± SD; n = 4 mice per genotype. (B) Pre- and postmitochondrial blocks in apoptosis modify the kinetics of ABT-737–induced thrombocytopenia. Mice were treated with a single dose of ABT-737, killed at time intervals, and platelet counts were determined at the indicated time intervals by automated counting. Data represent the mean ± SD; n = 2-6 mice/genotype per time point. (C) Caspase-9 deletion does not confer long-term resistance to ABT-737 in vivo. Circulating platelets were prelabeled with X488. Mice were then injected with a single dose of ABT-737. At the time points indicated, blood samples were obtained by tail bleeding and the presence of X488⁺ platelets was determined by flow cytometry. Data represent the mean ± SD; n = 5-7 mice per genotype; *P < .05, **P < .01.