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  4. Critical Role of Ena/VASP Proteins for Filopodia Formation in Neurons and in Function Downstream of Netrin-1

Critical Role of Ena/VASP Proteins for Filopodia Formation in Neurons and in Function Downstream of Netrin-1

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Author(s)
Lebrand, Cecile
•
Lanier, Lorene M.
•
Krause, Matthias
•
Svitkina, Tatyana M.
•
Borisy, Gary G.
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Dent, Erik W.
•
Strasser, Geraldine A.
•
Gertler, Frank
Date Issued
April 2004
Journal
Neuron
Publisher
Elsevier
Citation
Lebrand, Cecile, Erik W Dent, Geraldine A Strasser, Lorene M Lanier, Matthias Krause, Tatyana M Svitkina, Gary G Borisy, and Frank B Gertler. “Critical Role of Ena/VASP Proteins for Filopodia Formation in Neurons and in Function Downstream of Netrin-1.” Neuron 42, no. 1 (April 2004): 37-49. Copyright © 2004 Cell Press
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Final published version
Abstract
Ena/VASP proteins play important roles in axon outgrowth and guidance. Ena/VASP activity regulates the assembly and geometry of actin networks within fibroblast lamellipodia. In growth cones, Ena/VASP proteins are concentrated at filopodia tips, yet their role in growth cone responses to guidance signals has not been established. We found that Ena/VASP proteins play a pivotal role in formation and elongation of filopodia along neurite shafts and growth cone. Netrin-1-induced filopodia formation was dependent upon Ena/VASP function and directly correlated with Ena/VASP phosphorylation at a regulatory PKA site. Accordingly, Ena/VASP function was required for filopodial formation from the growth cone in response to global PKA activation. We propose that Ena/VASP proteins control filopodial dynamics in neurons by remodeling the actin network in response to guidance cues.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Terms of Use
Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
Persistent DSpace Link
http://hdl.handle.net/1721.1/83481
DOI of Published Version
https://doi.org/10.1016/S0896-6273(04)00108-4
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