COUP-TFI coordinates cortical patterning, neurogenesis, and laminar fate and modulates MAPK/ERK, AKT, and beta-catenin signaling

Cereb Cortex. 2008 Sep;18(9):2117-31. doi: 10.1093/cercor/bhm238. Epub 2007 Dec 28.

Abstract

A major unsolved question in cortical development is how proliferation, neurogenesis, regional growth, regional identity, and laminar fate specification are coordinated. Here we provide evidence, using loss-of-function and gain-of-function manipulations, that the COUP-TFI orphan nuclear receptor promotes ventral cortical fate, promotes cell cycle exit and neural differentiation, regulates the balance of early- and late-born neurons, and regulates the balanced production of different types of layer V cortical projection neurons. We suggest that COUP-TFI controls these processes by repressing Mapk/Erk, Akt, and beta-catenin signaling.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • COUP Transcription Factor I / genetics*
  • COUP Transcription Factor I / metabolism*
  • Cell Division / physiology
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Female
  • MAP Kinase Signaling System / physiology*
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Mitogen-Activated Protein Kinases / metabolism
  • Neocortex / cytology
  • Neocortex / embryology*
  • Neocortex / physiology*
  • Neurons / cytology
  • Neurons / physiology
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Stem Cells / cytology
  • Stem Cells / physiology
  • beta Catenin / metabolism*

Substances

  • COUP Transcription Factor I
  • CTNNB1 protein, mouse
  • beta Catenin
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • Extracellular Signal-Regulated MAP Kinases
  • Mitogen-Activated Protein Kinases