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LSD1-mediated demethylation of histone H3 lysine 4 triggers Myc-induced transcription

S Amente1, A Bertoni, A Morano

  • 1Department of Structural and Functional Biology, University of Naples 'Federico II', Naples, Italy.

Oncogene
|April 27, 2010
PubMed

Insights

Myc transcription factor recruits LSD1 to chromatin, causing DNA oxidation and recruiting repair enzymes. This process is crucial for activating Myc-target genes in cancer progression.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cancer Research

Background:

  • Myc is a key transcription factor driving cancer progression.
  • Myc binds to E-box DNA sequences (CACGTG) to regulate gene expression.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which Myc regulates gene transcription.
  • To investigate the role of LSD1 in Myc-mediated gene activation.

Main Methods:

  • Chromatin immunoprecipitation assays to detect protein-DNA interactions.
  • Biochemical assays to measure demethylation and oxidation.
  • Gene silencing and pharmacological inhibition to assess functional roles.

Main Results:

  • Myc recruits LSD1 to E-box chromatin, initiating transient H3K4 demethylation.
  • LSD1-mediated demethylation produces H2O2, causing guanine oxidation.
  • Oxidized guanine recruits OGG1 and Ape1, facilitating transcription initiation complex formation.
  • Inhibiting oxidation or silencing LSD1, OGG1, or Ape1 reduces Myc-target gene expression.

Conclusions:

  • Transient H3K4 demethylation by LSD1, coupled with local DNA oxidation, is essential for Myc-induced transcription.
  • This pathway highlights a novel mechanism linking epigenetic modification to DNA damage response in gene regulation.

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