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Related Experiment Videos

Multiple transcription factor binding sites mediate adenovirus E1A transactivation.

R Pei1, A J Berk

  • 1Department of Biological Chemistry, University of California, Los Angeles 90024-1570.

Journal of Virology
|August 1, 1989
PubMed
Summary

Adenovirus E1A protein transactivation depends on specific transcription factor binding sites. A single CREB/ATF or two E2F sites enable E1A response, while single Sp1 or E2F sites do not.

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Area of Science:

  • Molecular Biology
  • Virology
  • Gene Regulation

Background:

  • The adenovirus early region 1A (E1A) protein is crucial for viral gene expression.
  • Understanding how E1A interacts with host cell transcription factors is key to viral replication.
  • Synthetic promoter studies help elucidate the mechanisms of E1A-mediated transactivation.

Purpose of the Study:

  • To investigate the role of specific transcription factor binding sites in mediating adenovirus E1A transactivation.
  • To determine which DNA sequence motifs within promoter regions are responsive to E1A.
  • To compare the E1A responsiveness of different synthetic promoter constructs.

Main Methods:

  • Construction of viral mutants with substituted promoter regions (E1B, E4 TATA box).

Related Experiment Videos

  • Inclusion of specific transcription factor binding sites (CREB/ATF, Sp1, E2F) in synthetic promoters.
  • Assay of promoter activity and E1A response during early adenovirus infection.

    • Main Results:

    • A single CREB/ATF binding site conferred strong E1A responsiveness.
    • Two E2F binding sites, arranged similarly to the adenovirus type 2 E2 promoter, also mediated E1A transactivation.
    • A single Sp1 or E2F binding site, or the E4 TATA box, did not effectively mediate E1A response.
    • The E4 TATA box alone created a stronger basal promoter but lacked E1A responsiveness.

    Conclusions:

    • Specific transcription factor binding sites, including CREB/ATF and E2F, are essential for E1A-mediated transactivation.
    • The number and arrangement of binding sites significantly influence promoter response to E1A.
    • These findings provide direct evidence for the mechanism of E1A transactivation through distinct DNA elements.