Mediation of NGF signaling by post-translational inhibition of HES-1, a basic helix-loop-helix repressor of neuronal differentiation

Genes Dev. 1997 Dec 1;11(23):3168-81. doi: 10.1101/gad.11.23.3168.

Abstract

The induction of neurite outgrowth by NGF is a transcription-dependent process in PC12 cells, but the transcription factors that mediate this process are not known. Here we show that the bHLH transcriptional repressor HES-1 is a mediator of this process. Inactivation of endogenous HES-1 by forced expression of a dominant-negative protein induces neurite outgrowth in the absence of NGF and increases response to NGF. In contrast, expression of additional wild-type HES-1 protein represses and delays response to NGF. Endogenous HES-1 DNA-binding activity is post-translationally inhibited during NGF signaling in vivo, and phosphorylation of PKC consensus sites in the HES-1 DNA-binding domain inhibits DNA binding by purified HES-1 in vitro. Mutation of these sites generates a constitutively active protein that strongly and persistently blocks response to NGF. These results suggest that post-translational inhibition of HES-1 is both essential for and partially mediates the induction of neurite outgrowth by NGF signaling.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Basic Helix-Loop-Helix Transcription Factors
  • Cell Differentiation / physiology
  • DNA / metabolism
  • Enzyme Inhibitors / pharmacology
  • Gene Expression
  • Growth Inhibitors / antagonists & inhibitors
  • Growth Inhibitors / genetics
  • Growth Inhibitors / metabolism*
  • Helix-Loop-Helix Motifs*
  • Homeodomain Proteins / antagonists & inhibitors
  • Homeodomain Proteins / genetics
  • Homeodomain Proteins / metabolism*
  • Indoles / pharmacology
  • Maleimides / pharmacology
  • Mice
  • Nerve Growth Factors / metabolism*
  • Neurites
  • Neurons / cytology*
  • Neurons / drug effects
  • PC12 Cells
  • Phosphorylation
  • Protein Biosynthesis
  • Protein Kinase C / metabolism
  • Rats
  • Repressor Proteins / antagonists & inhibitors
  • Repressor Proteins / genetics
  • Repressor Proteins / metabolism*
  • Serine / metabolism
  • Signal Transduction*
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription Factor HES-1

Substances

  • Basic Helix-Loop-Helix Transcription Factors
  • Enzyme Inhibitors
  • Growth Inhibitors
  • Hes1 protein, mouse
  • Hes1 protein, rat
  • Homeodomain Proteins
  • Indoles
  • Maleimides
  • Nerve Growth Factors
  • Repressor Proteins
  • Transcription Factor HES-1
  • Serine
  • DNA
  • Protein Kinase C
  • bisindolylmaleimide
  • Tetradecanoylphorbol Acetate