Nature Cell Biology
7, 474 - 482 (2005)
Published online: 17 April 2005; | doi:10.1038/ncb1249
The KIF3 motor transports N-cadherin and organizes the developing neuroepitheliumJunlin Teng1, 3, Tatemitsu Rai1, 3, Yosuke Tanaka1, Yosuke Takei1, Takao Nakata1, Motoyuki Hirasawa2, 4, Ashok B. Kulkarni2
& Nobutaka Hirokawa11
Department of Cell Biology and Anatomy, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. 2
Functional Genomics Section, Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4326, USA. 3
These authors contributed equally to this work. 4
Current address is Department of Neurology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Correspondence should be addressed to Nobutaka Hirokawa hirokawa@m.u-tokyo.ac.jpIn the developing brain, the organization of the neuroepithelium is maintained by a critical balance between proliferation and cell−cell adhesion of neural progenitor cells. The molecular mechanisms that underlie this are still largely unknown. Here, through analysis of a conditional knockout mouse for the Kap3 gene, we show that post-Golgi transport of N-cadherin by the KIF3 molecular motor complex is crucial for maintaining this balance. N-cadherin and  -catenin associate with the KIF3 complex by co-immunoprecipitation, and colocalize with KIF3 in cells. Furthermore, in KAP3-deficient cells, the subcellular localization of N-cadherin was disrupted. Taken together, these results suggest a potential tumour-suppressing activity for this molecular motor.
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