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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2009.03.027 Byline: Jennifer C. Hocking (a), Carrie L. Hehr (a), Gabriel Bertolesi (a), Hiroshi Funakoshi (b), Toshikazu Nakamura (b), Sarah McFarlane (a) Keywords: Axon guidance; Development; Xenopus; Retina; Visual system; Growth cone; Bone morphogenetic protein Abstract: The actin cytoskeleton inside extending axonal and dendritic processes must undergo continuous assembly and disassembly. Some extrinsic factors modulate actin turnover through controlling the activity of LIM kinase 1 (LIMK1), which phosphorylates and inactivates the actin depolymerizing factor cofilin. Here, we for the first time examine the function and regulation of LIMK1 in vivo in the vertebrate nervous system. Upon expression of wildtype or kinase-dead forms of the protein, dendrite growth by Xenopus retinal ganglion cells (RGCs) was unchanged. In contrast, maintaining a low, but significant level, of LIMK1 function in the RGC axon is critical for proper extension. Interestingly, bone morphogenetic protein receptor II (BMPRII) is a major regulator of LIMK1 in extending RGC axons, as expression of a BMPRII lacking the LIMK1 binding region caused a dramatic shortening of the axons. Previously, we found that BMPRIIs stimulate dendrite initiation in vivo. Thus, the fact that manipulation of LIMK1 activity failed to alter dendrite growth suggests that BMPs may activate distinct signalling pathways in axons and dendrites. Author Affiliation: (a) Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada (b) Department of Biochemistry and Molecular Biology, Osaka University Graduate School of Medicine, Osaka, Japan Article History: Received 9 November 2008; Revised 26 March 2009; Accepted 30 March 2009