Fpn1 is not required for erythroid cell cycle progression although homozygous mutants are deficient in mitochondrial iron (Figure 2). (A) Fpn1 deficiency does not significantly increase erythroid cell death (percentage of cells with sub-G0/G1 DNA), but there are increased numbers of weh/+ and weh/weh embryos with increased numbers of percentage of sub-G0 DNA relative to vehicle-treated WT. Addition of 15 μM iron reduced cell death to WT levels. (B) weh/+ and weh/weh mutants did not differ from the WT group in the number of erythroid cells in G0/G1. This remained consistent with iron supplementation. (C) There were no significant differences between groups in the percentage of erythroid cells in S phase. (D) There were no significant differences between groups in the percentage of erythroid cells in G2/M. (E) Fpn1 deficiency increased cell death in nonerythroid (GFP⁻) cells. Addition of iron increased cell death in WT cells, so there were no differences in the percentage of nonerythroid cell with sub-G0/G1 between WT and mutant groups. (F) Fpn1 deficiency did not significantly decrease the proportion of nonerythroid cells in G0/G1. (G) There were no significant differences between groups in the percentage of erythroid cells in S phase. (H) There were no significant differences between groups in the percentage of nonerythroid cells in G2/M.