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Development ePress online publication date 29 Mar 2006
doi: 10.1242/dev.02330
Research article
Inactivation of aPKC
results in the loss of adherens junctions in neuroepithelial cells without affecting neurogenesis in mouse neocortex
Fumiyasu Imai,
Syu-ichi Hirai,
Kazunori Akimoto,
Hiromichi Koyama,
Takaki Miyata,
Masaharu Ogawa,
Shigeru Noguchi,
Toshikuni Sasaoka,
Tetsuo Noda,
and
Ohno Shigeo*
* Author for correspondence (e-mail: ohnos{at}med.yokohama-cu.ac.jp)
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.
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