TY - JOUR
T1 - β-globin gene promoter generates 5′ truncated transcripts in the embryonic/fetal erythroid environment
AU - Khazaie, Khashayarsha
AU - Gounari, Fotini
AU - Antoniou, Michael
AU - Deboer, Ernie
AU - Grosveld, Frank
N1 - Funding Information:
KJChazaie was supported by a Medical Research Council (UJC.) Recombinant Technology training fellowship. F.Gounari was supported by a Greek government training fellowship. We are grateful to Dr. Kristina Quade for the gift of cellular RNA from C57 BL/10 mouse embryos, and to Dr. Bjorn Vennstrom for allowing the completion of the final stages of this work in his laboratory.
PY - 1986/9/11
Y1 - 1986/9/11
N2 - 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.
AB - 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.
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U2 - 10.1093/nar/14.18.7199
DO - 10.1093/nar/14.18.7199
M3 - Article
C2 - 2429259
AN - SCOPUS:0023056962
SN - 0305-1048
VL - 14
SP - 7199
EP - 7212
JO - Nucleic acids research
JF - Nucleic acids research
IS - 18
ER -