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Published online
doi:10.1083/jcb.200906043
The Journal of Cell Biology, Vol. 188, No. 3, 429-441
The Rockefeller University Press, 0021-9525 $30.00
© Tamada et al.
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Article

Autonomous right-screw rotation of growth cone filopodia drives neurite turning



Atsushi Tamada1,2, Satoshi Kawase1, Fujio Murakami2,3, and Hiroyuki Kamiguchi1

1 Laboratory for Neuronal Growth Mechanisms, RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan
2 Division of Behavior and Neurobiology, National Institute for Basic Biology, Okazaki, Aichi 444-8585, Japan
3 Laboratory of Neuroscience, Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan

Correspondence to Atsushi Tamada: tamada{at}brain.riken.jp; or Hiroyuki Kamiguchi: kamiguchi{at}brain.riken.jp

The direction of neurite elongation is controlled by various environmental cues. However, it has been reported that even in the absence of any extrinsic directional signals, neurites turn clockwise on two-dimensional substrates. In this study, we have discovered autonomous rotational motility of the growth cone, which provides a cellular basis for inherent neurite turning. We have developed a technique for monitoring three-dimensional motility of growth cone filopodia and demonstrate that an individual filopodium rotates on its own longitudinal axis in the right-screw direction from the viewpoint of the growth cone body. We also show that the filopodial rotation involves myosins Va and Vb and may be driven by their spiral interactions with filamentous actin. Furthermore, we provide evidence that the unidirectional rotation of filopodia causes deflected neurite elongation, most likely via asymmetric positioning of the filopodia onto the substrate. Although the growth cone itself has been regarded as functionally symmetric, our study reveals the asymmetric nature of growth cone motility.

Abbreviations used in this paper: CCD, charge-coupled device; DIC, differential interference contrast; IRES, internal ribosomal entry site; mRFP, monomeric RFP; PDL, poly-D-lysine; Sema3F, semaphorin 3F.

© 2010 Tamada et al.
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