Mena Is Required for Neurulation and Commissure Formation
Name
Gertler_Mena is required.pdf
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Author(s)
Gates, Monte A
Witke, Walter
Macklis, Jeffrey D.
Kwiatkowski, David
Soriano, Philippe
Lanier, Lorene M.
Menzies, A. Sheila
Wehman, Ann M.
Gertler, Frank
Date Issued
February 1999
Journal
Neuron
Publisher
Elsevier
Citation
Lanier, Lorene M, Monte A Gates, Walter Witke, A.Sheila Menzies, Ann M Wehman, Jeffrey D Macklis, David Kwiatkowski, Philippe Soriano, and Frank B Gertler. “Mena Is Required for Neurulation and Commissure Formation.” Neuron 22, no. 2 (February 1999): 313-325. Copyright © 1999 Cell Press
Version
Final published version
Abstract
Mammalian enabled (Mena) is a member of a protein family thought to link signal transduction pathways to localized remodeling of the actin cytoskeleton. Mena binds directly to Profilin, an actin-binding protein that modulates actin polymerization. In primary neurons, Mena is concentrated at the tips of growth cone filopodia. Mena-deficient mice are viable; however, axons projecting from interhemispheric cortico-cortical neurons are misrouted in early neonates, and failed decussation of the corpus callosum as well as defects in the hippocampal commissure and the pontocerebellar pathway are evident in the adult. Mena-deficient mice that are heterozygous for a Profilin I deletion die in utero and display defects in neurulation, demonstrating an important functional role for Mena in regulation of the actin cytoskeleton.
MIT Department
Massachusetts Institute of Technology. Department of Biology
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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.
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DOI of Published Version
https://doi.org/10.1016/S0896-6273(00)81092-2
