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First published online 29 March 2006
doi: 10.1242/dev.02330

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Inactivation of aPKC results in the loss of adherens junctions in neuroepithelial cells without affecting neurogenesis in mouse neocortex

¹ Department of Molecular Biology, Yokohama City University Graduate School of Medical Science, 3-9 Fuku-ura, Kanazawa-ku, Yokohama 236-0004, Japan.
² College of Nursing, Yokohama City University Graduate School of Medical Science, 3-9 Fuku-ura, Kanazawa-ku, Yokohama 236-0004, Japan.
³ Department of Anatomy and Cell Biology, Graduate School of Medicine, Nagoya University, Nagoya 466-8550, Japan.
⁴ Laboratory for Cell Culture Development, Brain Science Institute, RIKEN, Saitama 351-0198, Japan.
⁵ Pharmaceutical Development Department, Meiji Dairies Co., 540 Naruda, Odawara, Kanagawa 250-0862, Japan.
⁶ National Institute for Basic Biology, National Institute of Natural Sciences Laboratory of Neurochemistry, Center for Transgenic Animals and Plants, 5-1 Higashiyama, Myodaiji, Okazaki 444-8787, Japan.
⁷ Department of Molecular Genetics, Tohoku University School of Medicine, Aoba-ku, Sendai, Miyagi 980-8575, Japan.

^* Author for correspondence (e-mail: ohnos{at}med.yokohama-cu.ac.jp)

Accepted 16 February 2006

In developing mammalian telencephalon, the loss of adherens junctions and cell cycle exit represent crucial steps in the differentiation of neuroepithelial cells into neurons, but the relationship between these cellular events remains obscure. Atypical protein kinase C (aPKC) is known to contribute to junction formation in epithelial cells and to cell fate determination for Drosophila neuroblasts. To elucidate the functions of aPKC, one out of two aPKC members, in mouse neocortical neurogenesis, a Nestin-Cre mediated conditional gene targeting system was employed. In conditional aPKC knockout mice, neuroepithelial cells of the neocortical region lost aPKC protein at embryonic day 15 and demonstrated a loss of adherens junctions, retraction of apical processes and impaired interkinetic nuclear migration that resulted in disordered neuroepithelial tissue architecture. These results are evidence that aPKC is indispensable for the maintenance of adherens junctions and may function in the regulation of adherens junction integrity upon differentiation of neuroepithelial cells into neurons. In spite of the loss of adherens junctions in the neuroepithelium of conditional aPKC knockout mice, neurons were produced at a normal rate. Therefore, we concluded that, at least in the later stages of neurogenesis, regulation of cell cycle exit is independent of adherens junctions.

Key words: aPKC, Cell polarity, Adherens junction, Neurogenesis, Brain

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