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Previous Article | Next Article
The Journal of Neuroscience, April 1, 2003, 23(7):2527
Control of Growth Cone Motility and Morphology by LIM Kinase and Slingshot via Phosphorylation and Dephosphorylation of Cofilin
Mitsuharu Endo1, Kazumasa Ohashi1, Yukio Sasaki2, Yoshio Goshima2, Ryusuke Niwa3, 4, Tadashi Uemura3, 4, and Kensaku Mizuno1 1 Department of Biomolecular Sciences, Graduate School of Life Sciences, Tohoku University, Sendai 980-8578, Japan, 2 Department of Pharmacology, Yokohama City University School of Medicine, Yokohama 236-0004, Japan, 3 Department of Molecular Genetics, The Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan, and 4 Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Kawaguchi 332-0012
Growth cone motility and morphology are based on actin-filament dynamics. Cofilin plays an essential role for the rapid turnover of actin filaments by severing and depolymerizing them. The activity of cofilin is repressed by phosphorylation at Ser3 by LIM kinase (LIMK, in which LIM is an acronym of the three gene products Lin-11, Isl-1, and Mec-3) and is reactivated by dephosphorylation by phosphatases, termed Slingshot (SSH). We investigated the roles of cofilin, LIMK, and SSH in the growth cone motility and morphology and neurite extension by expressing fluorescence protein-labeled cofilin, LIMK1, SSH1, or their mutants in chick dorsal root ganglion (DRG) neurons and then monitoring live images of growth cones by time-lapse video fluorescence microscopy. The expression of LIMK1 remarkably repressed growth cone motility and neurite extension, whereas the expression of SSH1 or a nonphosphorylatable S3A mutant of cofilin enhanced these events. The fan-like shape of growth cones was disorganized by the expression of any of these proteins. The repressive effects on growth cone behavior by LIMK1 expression were significantly rescued by the coexpression of S3A-cofilin or SSH1. These findings suggest that LIMK1 and SSH1 play critical roles in controlling growth cone motility and morphology and neurite extension by regulating the activity of cofilin and may be involved in signaling pathways that regulate stimulus-induced growth cone guidance. Using various mutants of cofilin, we also obtained evidence that the actin-filament-severing activity of cofilin is critical for growth cone motility and neurite extension.
Key words: LIM kinase; Slingshot; cofilin; actin-depolymerizing factor; growth cone guidance; neurite outgrowth
Copyright © 2003 Society for Neuroscience 0270-6474/03/2372527-11$05.00/0
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