The adenovirus EIIA enhancer. Analysis of regulatory sequences and changes in binding activity of ATF and EIIF following adenovirus infection.
Adenovirus EIIA upstream sequences which contain the binding sites for proteins ATF and EIIF act as an enhancer and can be trans-activated by both E1A and SV40 T/t-antigens. Specific mutation of either the ATF or EIIF binding site demonstrates that both act as positive regulators, decreasing transcription greater than 10-fold. Mutation of both the ATF and EIIF binding sites inhibited the EIIA enhancer 200-fold. Analysis of insertion mutations suggests that the spatial alignment of the upstream ATF and EIIF binding sites with respect to the downstream EIIF binding site on the DNA helix is important. Consistent with previous findings, using gel shift analysis we demonstrate that the binding activity of EIIF is increased following wild-type adenovirus infection. In contrast, using identical gel shift conditions, the binding activity of ATF is decreased by viral infection.
Loeken
M R
MR
Laboratory of Molecular Virology, National Cancer Institute, Bethesda, Maryland 20892.
Brady
J
J
D017456:Adenovirus Early Proteins; D000260:Adenoviruses, Human / Q000235:genetics*; D004268:DNA-Binding Proteins / Q000502:physiology; D004742:Enhancer Elements, Genetic; D005786:Gene Expression Regulation; D006367:HeLa Cells; D009690:Nucleic Acid Conformation; D009856:Oncogene Proteins, Viral / Q000502:physiology*; D011401:Promoter Regions, Genetic; D012045:Regulatory Sequences, Nucleic Acid; D014157:Transcription Factors / Q000502:physiology*; D014158:Transcription, Genetic
D017456:Adenovirus Early Proteins; D004268:DNA-Binding Proteins; D009856:Oncogene Proteins, Viral; D014157:Transcription Factors