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Neural Plasticity
Volume 2015, Article ID 947423, 13 pages
Research Article

CRMP4 and CRMP2 Interact to Coordinate Cytoskeleton Dynamics, Regulating Growth Cone Development and Axon Elongation

1Department of Anatomy, Medical College of Jinan University, Guangzhou 510630, China
2Postdoctoral Stations of Integrated Traditional and Western Medicine, Medical College of Jinan University, Guangzhou 510630, China
3Department of Pediatrics, The First Affiliated Hospital of Jinan University, Guangzhou 510630, China
4Department of Pediatrics, Guangzhou Women and Children’s Medical Center, The Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China
5Department of Pathophysiology, Medical College of Jinan University, Guangzhou 510630, China

Received 22 December 2014; Revised 13 April 2015; Accepted 15 April 2015

Academic Editor: Clive R. Bramham

Copyright © 2015 Minghui Tan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cytoskeleton dynamics are critical phenomena that underpin many fundamental cellular processes. Collapsin response mediator proteins (CRMPs) are highly expressed in the developing nervous system, mediating growth cone guidance, neuronal polarity, and axonal elongation. However, whether and how CRMPs associate with microtubules and actin coordinated cytoskeletal dynamics remain unknown. In this study, we demonstrated that CRMP2 and CRMP4 interacted with tubulin and actin in vitro and colocalized with the cytoskeleton in the transition-zone in developing growth cones. CRMP2 and CRMP4 also interacted with one another coordinately to promote growth cone development and axonal elongation. Genetic silencing of CRMP2 enhanced, whereas overexpression of CRMP2 suppressed, the inhibitory effects of CRMP4 knockdown on axonal development. In addition, knockdown of CRMP2 or overexpression of truncated CRMP2 reversed the promoting effect of CRMP4. With the overexpression of truncated CRMP2 or CRMP4 lacking the cytoskeleton interaction domain, the promoting effect of CRMP was suppressed. These data suggest a model in which CRMP2 and CRMP4 form complexes to bridge microtubules and actin and thus work cooperatively to regulate growth cone development and axonal elongation.