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