Regulation of transcription by AMP-activated protein kinase: phosphorylation of p300 blocks its interaction with nuclear receptors

J Biol Chem. 2001 Oct 19;276(42):38341-4. doi: 10.1074/jbc.C100316200. Epub 2001 Aug 22.

Abstract

AMP-activated protein kinase (AMP-kinase) modulates many metabolic processes in response to fluctuations in cellular energy status. Although most of its known targets are metabolic enzymes, it has been proposed that AMP-kinase might also regulate gene expression. Here we demonstrate that the transcriptional coactivator p300 is a substrate of AMP-kinase. Phosphorylation of p300 at serine 89 by AMP-kinase dramatically reduced its interaction, in vitro and in vivo, with the nuclear receptors peroxisome proliferator-activated receptor gamma, thyroid receptor, retinoic acid receptor, and retinoid X receptor, but did not affect its interaction with the non-nuclear receptor transcription factors E1a, p53, or GATA4. These findings indicate that the AMP-kinase signaling pathway selectively modulates a subset of p300 activities and represent the first example of a transcriptional component regulated by AMP-kinase. Our results suggest a direct link between cellular energy metabolism and gene expression.

MeSH terms

  • AMP-Activated Protein Kinases
  • Amino Acid Sequence
  • Animals
  • Blotting, Western
  • Cell Nucleus / metabolism*
  • Cricetinae
  • Dose-Response Relationship, Drug
  • Humans
  • Molecular Sequence Data
  • Multienzyme Complexes / metabolism*
  • Mutation
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Phosphorylation
  • Plasmids / metabolism
  • Protein Serine-Threonine Kinases / metabolism*
  • Receptors, Retinoic Acid / metabolism
  • Retinoid X Receptors
  • Sequence Homology, Amino Acid
  • Signal Transduction
  • Trans-Activators / genetics
  • Trans-Activators / metabolism*
  • Transcription Factors / metabolism
  • Transcription, Genetic*
  • Transfection
  • Two-Hybrid System Techniques

Substances

  • Multienzyme Complexes
  • Nuclear Proteins
  • Receptors, Retinoic Acid
  • Retinoid X Receptors
  • Trans-Activators
  • Transcription Factors
  • Protein Serine-Threonine Kinases
  • AMP-Activated Protein Kinases