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p63 and p73 transcriptionally regulate genes involved in DNA repair

Yu-Li Lin1, Shomit Sengupta, Katherine Gurdziel

  • 1Department of Molecular and Cellular Oncology, Graduate School of Biomedical Sciences, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, United States of America.

Plos Genetics
|October 10, 2009
PubMed

Insights

The p63 and p73 proteins regulate unique genes involved in DNA repair, distinct from p53. Loss of p63 and p73 impairs DNA repair and leads to mammary tumors, suggesting a tumor-suppressive role.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • The p53 protein family plays a crucial role in DNA damage response.
  • p63 and p73, while related to p53, possess unique functions in development and metastasis.
  • The specific transcriptional networks regulated by p63 and p73 remain largely uncharacterized.

Purpose of the Study:

  • To identify genes uniquely regulated by p63 and p73 in response to DNA damage.
  • To elucidate the distinct transcriptional roles of p63 and p73 compared to p53.
  • To investigate the involvement of p63 and p73 in DNA repair and tumor suppression.

Main Methods:

  • Genome-wide analysis of cells lacking p53 family members after DNA damage treatment.
  • Identification and validation of direct transcriptional targets of p63 and p73.
  • Assessment of DNA repair capacity in cells deficient for p63 and p73.
  • Tumorigenesis studies in mice with deficiencies in p63 and p73.

Main Results:

  • Over 100 genes in multiple pathways were uniquely regulated by p63 or p73, not p53.
  • BRCA2, Rad51, and mre11 were identified as direct transcriptional targets of p63 and p73.
  • Cells lacking p63 and p73 exhibited impaired DNA repair.
  • Mice heterozygous for p63 and p73 developed mammary tumors.

Conclusions:

  • p63 and p73 control a unique transcriptional network distinct from p53.
  • p63 and p73 are crucial for efficient DNA repair.
  • p63 and p73 act as tumor suppressors, particularly in mammary tumorigenesis.

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