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A p53-CBP/p300 transcription module is required for GAP-43 expression, axon outgrowth, and regeneration

A Tedeschi1, T Nguyen, R Puttagunta

  • 1Laboratory for NeuroRegeneration and Repair, Department of Neurology, Hertie Institute for Clinical Brain Research, University of Tuebingen, Otfried-Mueller Strasse 27, Tuebingen, Germany.

Cell Death and Differentiation
|December 6, 2008
PubMed

Insights

The tumor suppressor p53 and its partners CBP/p300 form a complex that drives axon regeneration by regulating the GAP-43 gene. This p53/GAP-43 pathway is crucial for nerve repair.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Transcription is vital for axon outgrowth and regeneration.
  • Specific transcription complexes regulating axon growth genes remain largely uncharacterized.

Purpose of the Study:

  • To identify transcription complexes controlling axon growth genes.
  • To investigate the role of p53 in regulating axon regeneration via GAP-43.

Main Methods:

  • Investigated the p53/CBP/p300 complex interaction.
  • Analyzed acetylated p53 (K372-382) binding to the GAP-43 promoter.
  • Utilized in vivo chromatin immunoprecipitation (ChIP) in an axon regeneration model.
  • Compared wild-type and p53 null mice for axon regeneration capacity.

Main Results:

  • The p53/CBP/p300 complex regulates the expression of growth-associated protein 43 (GAP-43).
  • Acetylated p53 (K372-382) promotes axon outgrowth and GAP-43 expression by binding the GAP-43 promoter.
  • p53 and CBP are induced post-axotomy, with increased p53 binding to the GAP-43 promoter.
  • The p53/GAP-43 transcriptional module is essential for in vivo axon regeneration.

Conclusions:

  • p53 acetylation and its complex with CBP/p300 are key regulators of axon regeneration through the GAP-43 gene.
  • This study reveals a novel molecular mechanism for nerve repair.
  • The p53/GAP-43 pathway presents potential therapeutic targets for enhancing axon regeneration.

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