We report here the localisation of sequences responsible for the faulty expression of human β-globin gene in Putko and K562 cells. Complete β-globin gene introduced into these cells produces transcripts with abnormal 5′ ends, while cotransfected mouse H2 gene is expressed correctly. Using hybrid constructs of these two genes we demonstrate that aberrant activity is conferred by sequences 5′ of the β-globin gene. Thus β-globin promoter attached to the H2 coding sequence produces H2 transcripts with truncated 5′ ends. By introducing a series of deletions in the )β-globin promoter we restrict these sequences to the -77 / +28 base pair region spanning the CAAT element to the translation initiation she. These results are consistent with the lack of recognition of the β-globin gene major cap site in Putko and K562 cells. We suggest that inactivity of the adult giobin gene in the embryonic/fetal environment is at least in part conferred by sequences within the β-giobin gene promoter.
ASJC Scopus subject areas