The human
alpha-globin-like embryonic
zeta-globin chains are present in abundance during the first 5 to 6 weeks of gestation. Subsequently,
zeta-globin chains are present in fetal blood at a very low level, which is supplanted by the expression of
alpha-globin chains. Adult individuals who are carriers of the (--SEA/)
alpha-thalassemia deletion, in contrast to normal adults, have low levels of embryonic
zeta-globin chains in their circulating erythrocytes. In this investigation, we constructed stable mouse-human hybrid cells with murine
erythroleukemia cells bearing human chromosome 16, with either the normal
alpha-globin gene cluster (alpha alpha/) or the (--SEA/) type of
alpha-thalassemia deletion. The results on the human
zeta-globin gene expression in these hybrid cells indicate that murine adult erythroid
transcription factors can induce the expression of human embryonic
zeta-globin gene is cis to the (--SEA/) deletion, in parallel with the endogenous mouse
alpha-globin gene expression. These data also show the importance of the DNA sequences within the (--SEA) deletion in regulating the expression of
zeta-globin gene in cis during normal human
hemoglobin ontogeny.