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

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...

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Published in:Journal of neural transplantation & plasticity 2015-01, Vol.2015 (2015), p.531-543-147
Main Authors: Guo, Guoqing, Wu, Fengming, Li, Sumei, Zhang, Jifeng, Ye, Yongheng, Cha, Caihui, Tan, Minghui, Gong, Sitang
Format: Article
Language:English
Subjects:
Actins - metabolism
Amino acids
Animals
Antibodies
Axons
Calcium phosphates
Cell adhesion & migration
Cell interaction
Cells, Cultured
Cytoskeleton
Cytoskeleton - metabolism
Experiments
Gene Knockdown Techniques
Growth Cones - metabolism
Hippocampus - metabolism
Laboratory animals
Microtubules - metabolism
Nerve Tissue Proteins - genetics
Nerve Tissue Proteins - metabolism
Neurons
Plasmids
Proteins
Rats, Sprague-Dawley
Tubulin - metabolism
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Summary: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.
ISSN:0792-8483
2090-5904
1687-5443
DOI:10.1155/2015/947423