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Regulation of iron transport is required for terminal erythroid differentiation even under iron-replete conditions that are sufficient for hemoglobinization

Erythroid cells are the main driver of iron utilization in vertebrates, as their main role is to synthesize hemoglobin to oxygenate the body’s tissues. As such, iron is a key nutrient for the development and function of erythroid cells. When iron deficient, erythroid cells are both lacking in hemoglobin and exhibit differentiation defects. Currently, the efficacy of iron supplementation is monitored by measuring indices of erythroid hemoglobinization. However, its effect on erythroid differentiation is less clear. In this study, we used zebrafish with genetic iron metabolism defects to determine if iron supplementation could rescue erythropoietic defects in organisms that are iron deficient at the cellular and systemic level. To carry out this study, we developed a technique to sort Tg(globin lcr:EGFP) erythrocytes from single zebrafish embryos onto slides for imaging. We found that iron supplementation in mfrn1 mutant zebrafish, which carry a defect in mitochondrial iron trafficking, restored hemoglobinization but not erythroid cell number or terminal differentiation. Iron supplementation in fpn1 mutant zebrafish, which have defects in export of iron from yolk syncytial cells and intestinal epithelium, functioning a model of dietary iron deficiency, restored erythroid cell number but not terminal differentiation deficiencies. Our data suggests that in addition to adequate iron levels, correct regulation of iron trafficking is required for optimal erythroid iron utilization and terminal erythropoiesis.