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Midbody and primary cilium of neural progenitors release extracellular membrane particles enriched in the stem cell marker prominin-1

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Dubreuil,  Veronique
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Marzesco,  Anne-Marie
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Corbeil,  Denis
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Huttner,  Wieland B.
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Wilsch-Brauninger,  Michaela
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Citation

Dubreuil, V., Marzesco, A.-M., Corbeil, D., Huttner, W. B., & Wilsch-Brauninger, M. (2007). Midbody and primary cilium of neural progenitors release extracellular membrane particles enriched in the stem cell marker prominin-1. Journal of Cell Biology, 176(4), 483-495.


Cite as: https://hdl.handle.net/21.11116/0000-0001-0F5A-B
Abstract
Expansion of the neocortex requires symmetric divisions of neuroepithelial cells, the primary progenitor cells of the developing mammalian central nervous system. Symmetrically dividing neuroepithelial cells are known to form a midbody at their apical (rather than lateral) surface. We show that apical midbodies of neuroepithelial cells concentrate prominin-1 (CD133), a somatic stem cell marker and defining constituent of a specific plasma membrane microdomain. Moreover, these apical midbodies are released, as a whole or in part, into the extracellular space, yielding the prominin-1-enriched membrane particles found in the neural tube fluid. The primary cilium of neuroepithelial cells also concentrates prominin-1 and appears to be a second source of the prominin-1-bearing extracellular membrane particles. Our data reveal novel origins of extracellular membrane traffic that enable neural stem and progenitor cells to avoid the asymmetric inheritance of the midbody observed for other cells and, by releasing a stem cell membrane microdomain, to potentially influence the balance of their proliferation versus differentiation.