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Essential role for the interaction between hnRNP H/F and a G quadruplex in maintaining p53 pre-mRNA 3'-end processing

Adrien Decorsière1, Anne Cayrel, Stéphan Vagner

  • 1INSERM U563, Institut Claudius Regaud, Toulouse, France.

Genes & Development
|February 4, 2011
PubMed

Insights

DNA damage typically halts mRNA processing. However, cells utilize a G-quadruplex and hnRNP H/F interaction to enable p53 mRNA 3'-end formation, crucial for apoptosis.

Area of Science:

  • Molecular Biology
  • Cellular Stress Response
  • Gene Regulation

Background:

  • DNA damage inhibits general mRNA 3'-end formation, repressing mRNA synthesis.
  • Understanding how p53 mRNA processing is regulated under these conditions is critical.

Purpose of the Study:

  • To investigate the mechanism of p53 mRNA 3'-end formation in DNA-damaged cells.
  • To identify how p53 expression is maintained when normal processing is inhibited.

Main Methods:

  • Analysis of pre-mRNA 3'-end processing regulation.
  • Investigating interactions between G-quadruplex structures and hnRNP H/F proteins.
  • Assessing the role of these interactions in p53 expression and apoptosis.

Main Results:

  • A G-quadruplex downstream of the p53 cleavage site interacts with hnRNP H/F.
  • This interaction is essential for p53 mRNA 3'-end formation in damaged cells.
  • The interaction is critical for p53 expression and subsequent apoptosis.

Conclusions:

  • DNA-damaged cells employ a specific rescue mechanism for p53 mRNA 3'-end processing.
  • This mechanism allows for stress-induced p53 accumulation and its function in apoptosis.
  • Highlights a novel pathway for maintaining gene expression during cellular stress.

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