Letter abstract


Nature Cell Biology 10, 93 - 101 (2008)
Published online: 16 December 2007 | doi:10.1038/ncb1673

Neuroepithelial progenitors undergo LGN-dependent planar divisions to maintain self-renewability during mammalian neurogenesis

Daijiro Konno1,4, Go Shioi1,4, Atsunori Shitamukai1, Asako Mori1, Hiroshi Kiyonari2, Takaki Miyata3 & Fumio Matsuzaki1

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During mammalian development, neuroepithelial cells function as mitotic progenitors, which self-renew and generate neurons. Although spindle orientation is important for such polarized cells to undergo symmetric or asymmetric divisions1, 2, its role in mammalian neurogenesis remains unclear. Here we show that control of spindle orientation is essential in maintaining the population of neuroepithelial cells, but dispensable for the decision to either proliferate or differentiate. Knocking out LGN, (the G protein regulator)3, 4, randomized the orientation of normally planar neuroepithelial divisions. The resultant loss of the apical membrane from daughter cells frequently converted them into abnormally localized progenitors without affecting neuronal production rate. Furthermore, overexpression of Inscuteable5 to induce vertical neuroepithelial divisions shifted the fate of daughter cells. Our results suggest that planar mitosis ensures the self-renewal of neuroepithelial progenitors by one daughter inheriting both apical and basal compartments during neurogenesis.

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  1. Laboratory for Cell Asymmetry, Center for Developmental Biology, RIKEN, and CREST, Japan Science and Technology Corporation, RIKEN, 2-2-3 Minatojima-Minamimachi, Chuou-ku, Kobe 650-0047, Japan.
  2. Laboratory for Animal Resources and Genetic Engineering, Center for Developmental Biology, RIKEN, 2-2-3 Minatojima-Minamimachi, Chuou-ku, Kobe 650-0047, Japan.
  3. Department of Anatomy and Cell Biology, and CREST, Japan Science and Technology Corporation, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa, Nagoya, Aichi 466-8550, Japan.
  4. These authors contributed equally to this work.

Correspondence to: Fumio Matsuzaki1 e-mail: fumio@cdb.riken.jp



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