Disruption of PIT1 delays erythroid maturation in E12 and E14 fetal livers. (A) Quantification of Epo mRNAs in PIT1^+/+ and PIT1^Δ5/Δ5 E12 fetal livers by real-time PCR. Data indicate the means ± SEM of 5 animals per genotype. Significant differences from control (black bar) are indicated. *P < .05. (B,D) Representative flow cytometric analysis of E12 fetal liver cells from PIT1^+/+, PIT1^neo/neo, PIT1^neo/Δ5, and PIT1^Δ5/Δ5embryos (B) and E14.5 fetal liver cells from PIT1^+/+, PIT1^neo/Δ5 and PIT1^neo/neo embryos (D). R1-R5 populations correspond to erythroid cells at different stages of maturation. Percentages of labeled cells were calculated by taking into account the background labeling (baseline defined by omitting Ab). (C,E) Analysis of percentage of E12 (C) and E14.5 PIT1^+/+ (black diamonds), PIT1^neo/neo (gray squares), PIT1^neo/Δ5 (gray circles) and PIT1^Δ5/Δ5 (black triangles) fetal liver erythroid cells (E) in the different stages of maturation. Data indicate the means ± SEM of at least 3 independent experiments. Significant differences from PIT1^+/+ are indicated. *P < .05; **P < .01; ***P < .001.