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Related Experiment Videos

Mutant p53 forms a complex with Sp1 on HIV-LTR DNA.

A Chicas1, P Molina, J Bargonetti

  • 1Department of Biological Sciences, Institute for Biomolecular Structure and Function, Hunter College, 695 Park Avenue, New York, New York, 10021, USA.

Biochemical and Biophysical Research Communications
|December 19, 2000
PubMed
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Mutant p53 (His273) interacts with Sp1 bound to DNA, activating human immunodeficiency virus (HIV) transcription. This interaction suggests mutant p53 enhances HIV replication through a DNA-driven complex.

Area of Science:

  • Molecular Biology
  • Virology
  • Cancer Biology

Background:

  • Mutant p53 proteins are frequently found in cancers and can alter cellular functions.
  • Certain p53 mutants activate transcription from the human immunodeficiency virus long terminal repeat (HIV-LTR), promoting viral replication.
  • The Sp1-binding sites within the HIV-LTR are crucial for this observed activation.

Purpose of the Study:

  • To investigate the hypothesis that mutant p53 interacts with DNA-bound Sp1.
  • To determine if this interaction leads to increased transcription from Sp1-dependent promoters.
  • To elucidate the mechanism by which mutant p53 influences HIV-LTR transcription.

Main Methods:

  • Utilized the MDA-MB-468 breast cancer cell line expressing endogenous mutant p53(His273).

Related Experiment Videos

  • Employed dominant-negative inhibition using p53(Val135) to assess mutant p53's role in HIV-LTR transcription.
  • Performed HIV-LTR DNA affinity chromatography to detect protein interactions.
  • Assessed sequence-specific DNA binding of mutant p53 to a super consensus sequence (SCS).

    • Main Results:

    • Mutant p53(His273) was shown to activate HIV-LTR transcription in MDA-MB-468 cells.
    • HIV-LTR-directed transcription was inhibited by p53(Val135), confirming mutant p53's involvement.
    • Coelution of p53(His273) and Sp1 was observed using HIV-LTR DNA affinity chromatography.
    • Mutant p53(His273) demonstrated sequence-specific binding to the SCS, with Sp1 coeluting from this site.

    Conclusions:

    • Mutant p53(His273) directly binds to Sp1 when Sp1 is associated with DNA.
    • This interaction suggests a mechanism where mutant p53 enhances transcription from Sp1-dependent promoters, including the HIV-LTR.
    • Activated HIV-LTR transcription by mutant p53 likely occurs via a DNA-driven multi-protein complex involving Sp1.