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A ribonucleotide reductase gene involved in a p53-dependent cell-cycle checkpoint for DNA damage

H Tanaka1, H Arakawa, T Yamaguchi

  • 1Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Japan.

Nature
|March 15, 2000
PubMed

Insights

The p53R2 gene, induced by DNA damage, encodes a ribonucleotide reductase crucial for DNA repair. This discovery links p53 tumor suppression to DNA repair mechanisms.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • The p53 gene is frequently inactivated in human cancers, impacting cell cycle control and DNA repair.
  • Ribonucleotide reductase (R2) is essential for DNA synthesis during cell division.

Purpose of the Study:

  • To identify and characterize novel p53-inducible genes involved in DNA damage response.
  • To elucidate the role of p53R2 in the p53-dependent DNA damage checkpoint and tumor suppression.

Main Methods:

  • Differential display to identify p53-inducible genes in a human cancer cell line.
  • Analysis of p53R2 gene structure, including p53-binding sequences.
  • Assessing p53R2 expression and its functional impact on DNA repair and cell survival after genotoxin exposure.

Main Results:

  • A novel p53-inducible gene, p53R2, was isolated, showing similarity to the R2 subunit of ribonucleotide reductase.
  • p53R2 expression is induced by DNA-damaging agents (UV, gamma-irradiation, adriamycin) in a p53-dependent manner.
  • p53R2 induction promotes G2/M arrest and cell survival, while its inhibition impairs DNA repair and reduces cell survival.

Conclusions:

  • p53R2 encodes a functional ribonucleotide reductase directly involved in the p53-mediated DNA damage checkpoint.
  • The p53R2 discovery establishes a link between ribonucleotide reductase activity, DNA repair, and p53 tumor suppression.

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