EpoR-Cre–mediated deletion of Mcl1 leads to blockade early in erythrocyte development. (A-C) Mouse fetal liver cells were isolated from Mcl1^F/F EpoR-Cre⁺ or Mcl1^F/wt EpoR-Cre⁺ embryos on the indicated day, labeled with CD45, CD71, TER119, or Annexin V antibodies, and analyzed by flow cytometry. (A) CD45⁻ cells representing E11.5 (top panels), E13.5 (middle panels), and E15.5 (bottom panels) embryos. (B) Absolute cell numbers in each differentiation stage, as represented in (A). E11.5 (top panels), E13.5 (middle panels), and E15.5 (bottom panels) are shown (n ≥ 5 biological replicates with 4 embryos each). Data are mean ± standard error of the mean (SEM). **P < .1, ***P < .01, ****P < .001, 1-way analysis of variance with α = 0.05. (C) Annexin V⁺ (dead) cells in E13.5 Mcl1^F/F EpoR-Cre⁺ or Mcl1^F/wt EpoR-Cre⁺ fetal livers. Graph represents percentage relative to wild-type control (n > 13 embryos from 5 litters. *P < .5, **P < .01, ****P < .001, Student t test. Dashed line denotes fold change of 1. (D) Liver sections from representative embryos subjected to immunohistochemical staining for caspase-3 (left panels) and a glycophorin A–associated protein (TER119; right panel) (original magnification ×60). See "Materials and methods" for further details. (E) DNA from fetal liver cells isolated from Mcl1^F/F EpoR-Cre⁺ or Mcl1^F/wt EpoR-Cre⁺ embryos were analyzed by PCR. “Control” indicates PCR control and represents the expected banding pattern.