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An essential role for a MEK-C/EBP pathway during growth factor- regulated cortical neurogenesis

  1. Author:
    Menard, C.
    Hein, P.
    Paquin, A.
    Savelson, A.
    Yang, X. M.
    Lederfein, D.
    Barnabe-Heider, F.
    Mir, A. A.
    Sterneck, E.
    Peterson, A. C.
    Johnson, P. F.
    Vinson, C.
    Miller, F. D.

  2. Author Address

    Univ Toronto, Inst Res, Hosp Sick Children, 555 Univ Ave, Toronto, ON M5G 1X8, Canada Univ Toronto, Inst Res, Hosp Sick Children, Toronto, ON M5G 1X8, Canada McGill Univ, Ctr Neuronal Survival, Montreal Neurol Inst, Royal Victoria Hosp, Montreal, PQ, Canada McGill Univ, Brain Tumor Res Ctr, Montreal Neurol Inst, Royal Victoria Hosp, Montreal, PQ, Canada Natl Canc Inst, Frederick, MD 21702 USA NCI, NIH, Bethesda, MD 20892 USA Miller FD Univ Toronto, Inst Res, Hosp Sick Children, 555 Univ Ave, Toronto, ON M5G 1X8, Canada
    1. Year: 2002
  2. Journal: Neuron
    1. 36
    2. 4
    3. Pages: 597-610
  4. Type of Article: Article
  1. Abstract:

    Mammalian neurogenesis is determined by an interplay between intrinsic genetic mechanisms and extrinsic cues such as growth factors. Here, we have defined a signaling cascade, 6 MEK-C/EBP pathway, that is essential for cortical progenitor cells to become post-mitotic neurons. Inhibition of MEK or of the C/EBP family of transcription factors inhibits neurogenesis while expression of a C/EBPbeta mutant that is a phosphorylation- mimic at a MEK-Rsk site enhances neurogenesis. C/EBP mediates this positive effect by direct transcriptional I activation of neuron-specific genes such as Talpha1 alpha-tubulin. Conversely, inhibition of C/EBP-dependent transcription enhances CNTF-mediated generation of astrocytes from the same progenitor cells. Thus, activation of a MEK-C/EBP pathway enhances neurogenesis and inhibits gliogenesis, thereby providing a mechanism whereby growth factors can selectively bias progenitors to become neurons during development.

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