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Cited by 178

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

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

Imai, Fumiyasu, Hirai, Syu-ichi, Akimoto, Kazunori, Koyama, Hiromichi, Miyata, Takaki, Ogawa, Masaharu, Noguchi, Shigeru, Sasaoka, Toshikuni, Noda, Tetsuo, Ohno, Shigeo·2006·Development

Abstract

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 aPKCλ, one out of two aPKC members, in mouse neocortical neurogenesis, a Nestin-Cre mediated conditional gene targeting system was employed. In conditional aPKCλ knockout mice, neuroepithelial cells of the neocortical region lost aPKCλ 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 aPKCλ 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 aPKCλ 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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Metadata

Authors
Imai, F., Hirai, S.-I., Akimoto, K., Koyama, H., Miyata, T., Ogawa, M., Noguchi, S., Sasaoka, T., Noda, T., & Ohno, S.
Venue
Development
Published
2006-05-01
Volume
133
Issue
9
Pages
1735-1744
ISSN
  • 0950-1991 (ISSN-L)
  • 1477-9129
OpenAlex
W2147369750
Cited by
178
References
4
FWCI
4.27
Type
journal article
Language
en
Open access
closed

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