Rac1-dependent actin filament organization in growth cones is necessary for ?1-integrin-mediated advance but not for growth on poly-D-lysine
1998; Wiley; Volume: 37; Issue: 4 Linguagem: Inglês
10.1002/(sici)1097-4695(199812)37
ISSN1097-4695
AutoresThomas B. Kuhn, Michael D. Brown, James R. Bamburg,
Tópico(s)Axon Guidance and Neuronal Signaling
ResumoJournal of NeurobiologyVolume 37, Issue 4 p. 524-540 Rac1-dependent actin filament organization in growth cones is necessary for β1-integrin–mediated advance but not for growth on poly-D-lysine Thomas B. Kuhn, Thomas B. Kuhn Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado 80523Search for more papers by this authorMichael D. Brown, Michael D. Brown Department of Anatomy and Neurobiology, Colorado State University, Fort Collins, Colorado 80523Search for more papers by this authorJames R. Bamburg, Corresponding Author James R. Bamburg Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado 80523Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado 80523Search for more papers by this author Thomas B. Kuhn, Thomas B. Kuhn Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado 80523Search for more papers by this authorMichael D. Brown, Michael D. Brown Department of Anatomy and Neurobiology, Colorado State University, Fort Collins, Colorado 80523Search for more papers by this authorJames R. Bamburg, Corresponding Author James R. Bamburg Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado 80523Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado 80523Search for more papers by this author First published: 12 December 1998 https://doi.org/10.1002/(SICI)1097-4695(199812)37:4 3.0.CO;2-HCitations: 65AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Abstract The activity of filopodia and lamellipodia determines the advance, motility, adhesion, and sensory capacity of neuronal growth cones. The shape and dynamics of these highly motile structures originate from the continuous reorganization of the actin cytoskeleton in response to extracellular signals. The small GTPases, Rac1, Rho, and CDC42, regulate the organization of actin filament structures in nonneuronal cells; yet, their role in growth cone motility and neurite outgrowth is poorly understood. We investigated in vitro the function of Rac1 in neurite outgrowth and differentiation by introducing purified recombinant mutants of Rac1 into primary chick embryo motor neurons via trituration. Endogenous Rac1 was expressed in growth cone bodies as well as in the tips and shafts of filopodia, where it often colocalized with actin filament structures. The introduction of constitutively active Rac1 resulted in an increase in rhodamine–phalloidin staining, presumably from an accumulation of actin filaments in growth cones, while dominant negative Rac1 caused a decrease in rhodamine–phalloidin staining. Nevertheless, both Rac1 mutants retarded growth cone advance, and hence attenuated neurite outgrowth and inhibited differentiation of neurites into axons and dendrites on laminin and fibronectin. In contrast, on poly-D-lysine, neither Rac1 mutant affected growth cone advance, neurite outgrowth, or neurite differentiation despite inducing similar changes in the amount of rhodamine–phalloidin staining in growth cones. Our data demonstrate that Rac1 regulates actin filament organization in neuronal growth cones and is pivotal for β1 integrin–mediated growth cone advance, but not for growth on poly-D lysine. © 1998 John Wiley & Sons, Inc. J Neurobiol 37: 524–540, 1998 Citing Literature Volume37, Issue4December 1998Pages 524-540 RelatedInformation
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