Vinexin beta interacts with the non-phosphorylated AF-1 domain of retinoid receptor gamma (RARgamma) and represses RARgamma-mediated transcription

J Biol Chem. 2005 Apr 29;280(17):17027-37. doi: 10.1074/jbc.M501344200. Epub 2005 Feb 25.

Abstract

Nuclear retinoic acid receptors (RARs) are ligand-dependent transcription factors that regulate the expression of retinoic acid target genes. Although the importance of RAR phosphorylation in their N-terminal domain is clearly established, the underlying mechanism for the phosphorylation-dependent transcriptional activity of the receptors had not been elucidated yet. Here, using a yeast two-hybrid system, we report the isolation of vinexin beta as a new cofactor that interacts with the N-terminal A/B domain of the RARgamma isotype. Vinexin beta is a multiple SH3 motif-containing protein associated with the cytoskeleton and also present in the nucleus. We demonstrate that vinexin beta colocalizes with RARgamma in the nucleus and interacts with the non-phosphorylated form of the AF-1 domain of RARgamma. We also show that this interaction is prevented upon phosphorylation of the AF-1 domain. Using F9 cells stably overexpressing vinexin beta or vinexin knockdown by RNA interference, we demonstrate that vinexin beta is an inhibitor of RARgamma-mediated transcription. We propose a model in which phosphorylation of the AF-1 domain controls RARgamma-mediated transcription through triggering the dissociation of vinexin beta.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / chemistry
  • Adaptor Proteins, Signal Transducing / metabolism*
  • Amino Acid Motifs
  • Amino Acid Sequence
  • Animals
  • COS Cells
  • Cell Nucleus / metabolism
  • Chloramphenicol O-Acetyltransferase / metabolism
  • Cloning, Molecular
  • DNA, Complementary / metabolism
  • Glutathione Transferase / metabolism
  • Humans
  • Immunoprecipitation
  • Mice
  • Microscopy, Fluorescence
  • Molecular Sequence Data
  • Muscle Proteins / chemistry
  • Muscle Proteins / metabolism*
  • Phosphorylation
  • Plasmids / metabolism
  • Protein Binding
  • Protein Structure, Tertiary
  • RNA / metabolism
  • RNA Interference
  • RNA, Small Interfering / metabolism
  • Receptors, Retinoic Acid / chemistry*
  • Retinoic Acid Receptor gamma
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sequence Homology, Amino Acid
  • Time Factors
  • Transcription, Genetic*
  • Transcriptional Activation
  • Transfection
  • Tretinoin / metabolism
  • Two-Hybrid System Techniques
  • beta-Galactosidase / metabolism
  • src Homology Domains

Substances

  • Adaptor Proteins, Signal Transducing
  • DNA, Complementary
  • Muscle Proteins
  • RNA, Small Interfering
  • Receptors, Retinoic Acid
  • SORBS3 protein, human
  • Sorbs3 protein, mouse
  • Tretinoin
  • RNA
  • Chloramphenicol O-Acetyltransferase
  • Glutathione Transferase
  • beta-Galactosidase