AMPK regulates histone H2B O-GlcNAcylation

Nucleic Acids Res. 2014 May;42(9):5594-604. doi: 10.1093/nar/gku236. Epub 2014 Apr 1.

Abstract

Histone H2B O-GlcNAcylation is an important post-translational modification of chromatin during gene transcription. However, how this epigenetic modification is regulated remains unclear. Here we found that the energy-sensing adenosine-monophosphate-activated protein kinase (AMPK) could suppress histone H2B O-GlcNAcylation. AMPK directly phosphorylates O-linked β-N-acetylglucosamine (O-GlcNAc) transferase (OGT). Although this phosphorylation does not regulate the enzymatic activity of OGT, it inhibits OGT-chromatin association, histone O-GlcNAcylation and gene transcription. Conversely, OGT also O-GlcNAcylates AMPK and positively regulates AMPK activity, creating a feedback loop. Taken together, these results reveal a crosstalk between the LKB1-AMPK and the hexosamine biosynthesis (HBP)-OGT pathways, which coordinate together for the sensing of nutrient state and regulation of gene transcription.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • AMP-Activated Protein Kinases / physiology*
  • Acetylglucosamine / metabolism
  • Chromatin / metabolism
  • Energy Metabolism
  • Epigenesis, Genetic
  • Glycosylation
  • Hep G2 Cells
  • Histones / metabolism*
  • Homeostasis
  • Humans
  • N-Acetylglucosaminyltransferases / metabolism
  • Phosphorylation
  • Protein Processing, Post-Translational*
  • Transcription, Genetic

Substances

  • Chromatin
  • Histones
  • N-Acetylglucosaminyltransferases
  • AMP-Activated Protein Kinases
  • PRKAA1 protein, human
  • Acetylglucosamine