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MBC in Press, published online ahead of print August 15, 2007
Mol. Biol. Cell 10.1091/mbc.E07-04-0372

A more recent version of this article appeared on November 1, 2007
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Submitted on April 25, 2007
Revised on July 23, 2007
Accepted on August 8, 2007

Neurabin-I Is Phosphorylated by Cdk5: Implications for Neuronal Morphogenesis and Cortical Migration

Frédéric Causeret,* Tom Jacobs,* Mami Terao,{dagger} Owen Heath,* Mikio Hoshino,{dagger} and Margareta Nikolic*

*Department of Cellular and Molecular Neuroscience, Imperial College School of Medicine, Charing Cross Campus, London W6 8RP, United Kingdom; {dagger}Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan

Monitoring Editor: Paul Forscher

The correct morphology and migration of neurones, which is essential for the normal development of the nervous system, is enabled by the regulation of their cytoskeletal elements. We reveal that Neurabin-I, a neuronal specific F-actin binding protein, has an essential function in the developing forebrain. We show that gain and loss of Neurabin-I expression affect neuronal morphology, neurite outgrowth and radial migration of differentiating cortical and hippocampal neurones, suggesting that tight regulation of Neurabin-I function is required for normal forebrain development. Importantly, loss of Neurabin-I prevents pyramidal neurones from migrating into the cerebral cortex, indicating its essential role during early stages of corticogenesis. We demonstrate that in neurones Rac1 activation is affected by the expression levels of Nb1. Furthermore, the Cdk5 kinase, a key regulator of neuronal migration and morphology, directly phosphorylates Neurabin-I and controls its association with F-actin. Mutation of the Cdk5 phosphorylation site reduces the phenotypic consequences of Neurabin-I overexpression both in vitro and in vivo, suggesting that Neurabin-I function depends, at least in part on its phosphorylation status. Together our findings provide new insight into the signaling pathways responsible for controlled changes of the F-actin cytoskeleton that are required for normal development of the forebrain.

Address correspondence to: Margareta Nikolic (m.nikolic{at}imperial.ac.uk)




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