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The Journal of Neuroscience, August 8, 2007, 27(32):8604-8615; doi:10.1523/JNEUROSCI.0765-07.2007

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Development/Plasticity/Repair
Localized Activation of p21-Activated Kinase Controls Neuronal Polarity and Morphology

Tom Jacobs,¹ Frédéric Causeret,¹ Yoshiaki V. Nishimura,² Mami Terao,² Adele Norman,¹ Mikio Hoshino,² and Margareta Nikoli¹

¹Department of Cellular and Molecular Neuroscience, Division of Neuroscience and Mental Health, Imperial College School of Medicine, Charing Cross Campus, London W6 8RP, United Kingdom, and ²Department of Pathology and Tumor Biology, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan

Correspondence should be addressed to Dr. Margareta Nikoli, Department of Cellular and Molecular Neuroscience, Division of Neuroscience and Mental Health, Imperial College School of Medicine, Charing Cross Campus, Fulham Palace Road, London W6 8RP, UK. Email: m.nikolic{at}imperial.ac.uk

In the developing forebrain, neuronal polarization is a stepwise and initially reversible process that underlies correct migration and axon specification. Many aspects of cytoskeletal changes that accompany polarization are currently molecularly undefined and thus poorly understood. Here we reveal that the p21-activated kinase (Pak1) is essential for the specification of an axon and dendrites. In hippocampal neurons, activation of Pak1 is spatially restricted to the immature axon despite its uniform presence in all neurites. Hyperactivation of Pak1 at the membrane of all neurites or loss of Pak1 expression disrupts both neuronal morphology and the distinction between an axon and dendrites. We reveal that Pak1 acts on polarity in a kinase-dependent manner, by affecting the F-actin and microtubule cytoskeleton at least in part through Rac1 and cofilin. Our data are the first to demonstrate the importance of localized Pak1 kinase activation for neuronal polarization and differentiation.

Key words: Pak1 kinase; polarity; neuron; cytoskeleton; F-actin; axon

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Received Feb. 20, 2007; revised May 31, 2007; accepted June 18, 2007.

Correspondence should be addressed to Dr. Margareta Nikoli, Department of Cellular and Molecular Neuroscience, Division of Neuroscience and Mental Health, Imperial College School of Medicine, Charing Cross Campus, Fulham Palace Road, London W6 8RP, UK. Email: m.nikolic{at}imperial.ac.uk

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