Regulation of neural progenitor proliferation by EGF signaling in the spinal cord

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  • Hayakawa-Yano Yoshika
    Department of Physiology, Keio University School of Medicine, Tokyo, Japan
  • Shimazaki Takuya
    Department of Physiology, Keio University School of Medicine, Tokyo, Japan Core Research for Evolutional Science Technology, Solution-Oriented Research for Science and Technology, Japan Science and Technology Agency, Saitama, Japan
  • Okano Hideyuki
    Department of Physiology, Keio University School of Medicine, Tokyo, Japan Core Research for Evolutional Science Technology, Solution-Oriented Research for Science and Technology, Japan Science and Technology Agency, Saitama, Japan

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A wide variety of neurons and glial cells are generated in the developing central nervous system (CNS). The precise regulation of cell-type determination and cell number is thought to be indispensable for the appropriate development and physiological functions of the CNS. Both extrinsic and intrinsic molecular mechanisms, which regulate timing and position in cytogenesis, enable the acquisition of diversity and the control of numbers in neurons and glial cells. The specification of neurons and glial cells in the embryonic spinal cord has been intensively studied. Distinct types of neurons and glial cells are generated along the dorsoventral axis of the embryonic spinal cord, which is regulated by extracellular molecules and transcriptional codes. However, the molecular mechanisms regulating cytogenesis of certain progenitor cells through extracellular molecules have been poorly elucidated. We have recently demonstrated that epidermal growth factor (EGF) signaling via Grb2 associated binder1 (Gab1) contributes to the proliferation of Olig2-positive progenitors that sequentially generate motoneuron and glial cells in the developing spinal cord, in a time and position-restricted manner. In this review, the molecular mechanisms of progenitor proliferation via EGF signaling will be discussed by focusing on the embryonic spinal cord.

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