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YY1 binding to a subset of p53 DNA-target sites regulates p53-dependent transcription

Tatiana Yakovleva1, Larissa Kolesnikova, Vladana Vukojević

  • 1Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.

Biochemical and Biophysical Research Communications
|May 4, 2004
PubMed

Insights

The transcription factor YY1 binds to some of the same DNA sites as the tumor suppressor p53. YY1 can inhibit p53-activated gene transcription, potentially influencing cell fate decisions like growth arrest or apoptosis.

Area of Science:

  • Molecular Biology
  • Gene Regulation
  • Cancer Biology

Background:

  • The tumor suppressor protein p53 is a key regulator of gene transcription, controlling cellular responses to stress.
  • p53 exerts its functions by binding to specific DNA sequences known as p53-binding sites.
  • The precise mechanisms by which p53 activity is modulated, especially in relation to other transcription factors, are not fully understood.

Purpose of the Study:

  • To identify other DNA-binding factors that interact with p53-target sites.
  • To investigate the functional consequence of co-occupancy of p53-binding sites by other factors.
  • To determine the role of the transcription regulator YY1 in p53-mediated gene expression.

Main Methods:

  • DNA-binding assays to identify factors binding to p53-target sequences.
  • Antibody reactivity and purified protein experiments for factor identification.
  • Site-directed mutagenesis to analyze the role of specific DNA sequences.
  • Transfection experiments to assess transcriptional activity.
  • Immunofluorescence microscopy to determine protein localization in apoptotic cells.

Main Results:

  • A subset of p53-binding sites is also recognized by the transcription factor YY1.
  • The YY1 core binding sequence (ACAT) is centrally located within p53-half-binding sites in genes like p21 and GADD45.
  • YY1 inhibits p53-activated transcription from p53-binding sites containing the ACAT sequence.
  • YY1 and p53 show co-localization in specific nuclear domains during apoptosis.

Conclusions:

  • YY1 acts as a repressor of p53-dependent transcription at a subset of p53-target genes.
  • The interaction between YY1 and p53 at specific DNA sites may play a critical role in determining cellular outcomes, such as growth arrest versus apoptosis.
  • This cross-regulation provides a potential mechanism for fine-tuning p53's tumor suppressor functions.

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