COUP-TFI coordinates cortical patterning, neurogenesis, and laminar fate and modulates MAPK/ERK, AKT, and beta-catenin signaling.
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.
Pubmed ID: 18165280 RIS Download
Animals | COUP Transcription Factor I | Cell Division | Extracellular Signal-Regulated MAP Kinases | Female | MAP Kinase Signaling System | Male | Mice | Mice, Inbred BALB C | Mice, Inbred C57BL | Mice, Transgenic | Mitogen-Activated Protein Kinases | Neocortex | Neurons | Phosphatidylinositol 3-Kinases | Proto-Oncogene Proteins c-akt | Stem Cells | beta Catenin