Erythroid cell iron uptake and globin synthesis were studied in the anemia of the Belgrade Laboratory rat (gene symbol, b), an autosomal recessive trait characterized by hypochromia and hyperferrinemia. Reticulocyte protein and globin synthesis, as measured in vitro by the incorporation of 3H-L-leucine, were significantly diminished in b/b animals, although no major imbalance between alpha-and beta-chain production was observed in b/b reticulocytes. The incorporation in vitro of 3H-L-methionine into marrow cell globin demonstrated no difference between b/b animals and +/? control animals in the proportion of alpha-to beta-chain production. The transfer of iron from plasma to reticulocytes, as measured in vitro by the uptake of 59Fe, was significantly decreased in b/b animals; Sephadex G 200 chromatography of b/b red cell lysates did not reveal the accumulation of 59Fe in nonhemoglobin fractions found when heme synthesis was inhibited with isoniazid. The magnitude of the reticulocyte iron-uptake defect was greater than the reticulocyte globin-synthesis defect, suggesting that the former is the primary lesion.