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DNA damage induced p53 downregulates Cdc20 by direct binding to its promoter causing chromatin remodeling

Taraswi Banerjee1, Somsubhra Nath, Susanta Roychoudhury

  • 1Molecular and Human Genetics Division, Indian Institute of Chemical Biology, Council of Scientific and Industrial Research, Kolkata 700032, India.

Nucleic Acids Research
|March 11, 2009
PubMed

Insights

The tumor suppressor p53 downregulates CDC20, a key cell cycle regulator, through direct promoter binding and chromatin remodeling. This mechanism helps maintain chromosomal stability, especially under genotoxic stress.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • CDC20 is crucial for the Spindle Assembly Checkpoint (SAC) and is overexpressed in tumors, leading to chromosomal instability.
  • The precise mechanisms by which SAC responds to genotoxic stress, particularly involving CDC20 regulation, remain incompletely understood.

Purpose of the Study:

  • To investigate how p53 influences Cdc20 transcription, especially in response to DNA damage.
  • To elucidate the molecular mechanisms underlying p53-mediated repression of Cdc20.

Main Methods:

  • Utilized ectopic p53 expression and DNA damage induction in cell models.
  • Performed p53-binding site identification and chromatin remodeling assays.
  • Analyzed Cdc20 promoter activity and regulation via CDE/CHR and CCAAT elements.

Main Results:

  • Ectopic or DNA damage-induced p53 transcriptionally downregulates Cdc20.
  • Identified and validated a functional p53-binding site on the Cdc20 promoter, leading to chromatin remodeling and repression.
  • p53 also represses Cdc20 via the CDE/CHR element independently of p21, but this is specific to p53 overexpression, not DNA damage.
  • CCAAT elements in the Cdc20 promoter are not utilized by p53 for downregulation.

Conclusions:

  • p53 acts as a transcriptional repressor of Cdc20 through distinct mechanisms involving direct promoter binding and chromatin modification.
  • These findings reveal a novel pathway for p53 in maintaining genomic stability by controlling CDC20 levels during genotoxic stress.

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