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p53-dependent repression of polo-like kinase-1 (PLK1)

Lynsey McKenzie1, Sharon King, Lynnette Marcar

  • 1Biomedical Research Institute, University of Dundee, Dundee, UK.

Cell Cycle (Georgetown, Tex.)
|October 22, 2010
PubMed

Insights

The tumor suppressor p53 directly represses Polo-like kinase 1 (PLK1) gene expression. This p53-mediated transcriptional repression of PLK1 is crucial for the DNA damage-induced G₂/M cell cycle arrest.

Area of Science:

  • Molecular Biology
  • Cell Cycle Regulation
  • Cancer Biology

Background:

  • Polo-like kinase 1 (PLK1) is essential for G₂/M cell cycle transition.
  • PLK1 is inactivated and depleted during the DNA damage-induced G₂/M checkpoint.
  • The tumor suppressor protein p53 plays a key role in cell cycle control and DNA damage response.

Purpose of the Study:

  • To elucidate the mechanism by which PLK1 expression is downregulated in response to DNA damage.
  • To determine the role of p53 in the transcriptional repression of PLK1.
  • To investigate the requirement of PLK1 for p53-mediated G₂/M cell cycle arrest.

Main Methods:

  • Chromatin immunoprecipitation (ChIP) assays to detect p53 binding to the PLK1 promoter.
  • Reporter gene assays to assess p53-mediated transcriptional repression of the PLK1 promoter.
  • RNA interference (RNAi) to silence PLK1 expression and assess its effect on cell cycle progression.
  • Treatment with histone deacetylase inhibitor (trichostatin A) to investigate the role of chromatin modification.

Main Results:

  • p53 directly represses PLK1 gene expression through transcriptional mechanisms, independent of p21.
  • p53 binds to two specific sites (p53RE1 and p53RE2) on the PLK1 promoter, with binding to p53RE2 enhanced by DNA damage.
  • Histone deacetylase recruitment to the PLK1 promoter is involved in p53-mediated repression.
  • Silencing PLK1 expression impairs cell cycle progression, confirming its role in the p53-mediated G₂/M checkpoint.

Conclusions:

  • PLK1 is a direct transcriptional target of p53.
  • p53-mediated repression of PLK1 is a critical mechanism for achieving G₂/M cell cycle arrest following DNA damage.
  • These findings identify a novel pathway in the p53-dependent DNA damage response.

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