Transferrin receptor gene is hyperexpressed and transcriptionally regulated in differentiating erythroid cells.

We have analyzed the developmental pattern of expression of the chicken transferrin receptor (CTR) gene in various chick embryonic tissues. Northern analyses of RNA from embryonic tissues at different stages of development and cultured chick embryonic fibroblasts (CEFs) show that CTR is hyperexpressed in differentiating erythroid cells such that the steady-state level of CTR mRNA in these cells could be 200 or more times higher than in nonerythroid cells. In vitro nuclear transcription assays using nuclei from embryonic erythroid and brain cells, as well as CEFs, demonstrate that the vast differences in CTR mRNA levels in these cells are reflected in their respective CTR gene transcriptional activities. During development, the steady-state level of CTR mRNA declines in all tissues and, in erythroid cells, this pattern is accompanied by a similar decline in beta-globin mRNA levels. These changes are concurrent with the decreases in CTR and beta-globin mRNA transcriptional activities during erythroid maturation. Taken together, our results indicate that the hyperexpression of the CTR gene in differentiating erythroid cells is regulated to a significant degree at the transcriptional level. We also demonstrate that, in erythroid cells, neither CTR gene transcription nor CTR mRNA stability is regulated by intracellular iron levels.