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p53 and Delta Np63 alpha differentially bind and regulate target genes involved in cell cycle arrest, DNA repair and

K L Schavolt1, J A Pietenpol

  • 1Department of Biochemistry, Center for Molecular Toxicology, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA.

Oncogene
|April 4, 2007
PubMed

Insights

The p53 family protein DeltaNp63alpha represses p53 target genes involved in cell cycle arrest, DNA repair, and apoptosis. Its binding and that of p53 change with genotoxic stress, impacting gene regulation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • The precise mechanisms governing p53 family protein regulation of target genes under cellular stress remain unclear.
  • Understanding these mechanisms is crucial for comprehending cellular responses to damage and stress.

Purpose of the Study:

  • To investigate the binding dynamics of p53 and DeltaNp63alpha to target gene regulatory regions.
  • To elucidate the role of DeltaNp63alpha in modulating p53-mediated gene expression.

Main Methods:

  • Chromatin immunoprecipitation was employed to assess protein binding in primary human epidermal keratinocytes (HEKs).
  • Microarray analysis was utilized to examine transcriptomic changes in response to p53 and DeltaNp63alpha expression.

Main Results:

  • DeltaNp63alpha constitutively binds to target gene sites in proliferating cells, while p53 binding varies.
  • Genotoxic stress alters p53 and DeltaNp63alpha occupancy, with p53 increasing and DeltaNp63alpha decreasing.
  • Microarray data revealed inverse regulation of specific genes by p53 and DeltaNp63alpha.

Conclusions:

  • DeltaNp63alpha acts as a repressor for select p53 target genes involved in critical cellular processes.
  • The location of p53 consensus binding sites may influence constitutive RNA polymerase II binding in proliferating cells.

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