Journal
CURRENT BIOLOGY
Volume 23, Issue 12, Pages 1046-1056Publisher
CELL PRESS
DOI: 10.1016/j.cub.2013.04.057
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Funding
- National Institutes of Health
- Muscular Dystrophy Association
- F32 fellowship award from National Institutes of Health
- National Institute of Neurological Disorders and Stroke [P30NS055077]
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Background: Actin-based cell motility is fundamental, for development, function, and malignant events in eukaryotic organisms. During neural development, axonal growth cones depend on rapid assembly and disassembly of actin filaments (F-actin) for their guided extension to specific targets for wiring. Monomeric globular actin (G-actin) is the building block for F-actin but is not considered to play a direct role in spatiotemporal control of actin dynamics in cell motility. Results: Here we report that a pool of G-actin dynamically localizes to the leading edge of growth cones and neuroblastoma cells to spatially elevate the G-/F-actin ratio that drives membrane protrusion and cell movement. Loss of G-actin localization leads to the cessation and retraction of membrane protrusions. Moreover, G-actin localization occurs asymmetrically in growth cones during attractive turning. Finally, we identify the actin monomer-binding proteins profilin and thymosin beta 4 as key molecules that localize actin monomers to the leading edge of lamellipodia for their motility. Conclusions: Our results suggest that dynamic localization of G-actin provides a novel mechanism to regulate the spatiotemporal actin dynamics underlying membrane protrusion in cell locomotion and growth cone chemotaxis.
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