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  4. Integrin Signaling Switches the Cytoskeletal and Exocytic Machinery that Drives Neuritogenesis

Integrin Signaling Switches the Cytoskeletal and Exocytic Machinery that Drives Neuritogenesis

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Author(s)
Gupton, Stephanie L.
•
Gertler, Frank
Date Issued
May 2010
Journal
Developmental Cell
Publisher
Elsevier B.V.
Citation
Gupton, Stephanie L., and Frank B. Gertler. “Integrin Signaling Switches the Cytoskeletal and Exocytic Machinery That Drives Neuritogenesis.” Developmental Cell 18.5 (2010): 725–736. Web.
Version
Author's final manuscript
Abstract
Neurons establish their unique morphology by elaborating multiple neurites that subsequently form axons and dendrites. Neurite initiation entails significant surface area expansion, necessitating addition to the plasma membrane. We report that regulated membrane delivery coordinated with the actin cytoskeleton is crucial for neuritogenesis, and identify two independent pathways that use distinct exocytic and cytoskeletal machinery to drive neuritogenesis. One pathway employs Ena/VASP-regulated actin dynamics coordinated with VAMP2-mediated exocytosis, and involves a novel role for Ena/VASP in exocytosis. A second mechanism occurs in the presence of laminin through integrin-dependent activation of FAK and src, and utilizes coordinated activity of the Arp2/3 complex and VAMP7-mediated exocytosis. We conclude that neuritogenesis can be driven by two distinct pathways that differentially coordinate cytoskeletal dynamics and exocytosis. These regulated changes and coordination of cytoskeletal and exocytic machinery may be utilized in other physiological contexts involving cell motility and morphogenesis.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Koch Institute for Integrative Cancer Research at MIT
Terms of Use
Creative Commons Attribution-Noncommercial-Share Alike 3.0
http://creativecommons.org/licenses/by-nc-sa/3.0/
Persistent DSpace Link
http://hdl.handle.net/1721.1/73488
DOI of Published Version
https://doi.org/10.1016/j.devcel.2010.02.017
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