Antagonism between Ena/VASP proteins and actin filament capping regulates fibroblast motility |
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Authors: | Bear James E Svitkina Tatyana M Krause Matthias Schafer Dorothy A Loureiro Joseph J Strasser Geraldine A Maly Ivan V Chaga Oleg Y Cooper John A Borisy Gary G Gertler Frank B |
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Institution: | Massachusetts Institute of Technology, Department of Biology, Cambridge 02139, USA. |
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Abstract: | Cell motility requires lamellipodial protrusion, a process driven by actin polymerization. Ena/VASP proteins accumulate in protruding lamellipodia and promote the rapid actin-driven motility of the pathogen Listeria. In contrast, Ena/VASP negatively regulate cell translocation. To resolve this paradox, we analyzed the function of Ena/VASP during lamellipodial protrusion. Ena/VASP-deficient lamellipodia protruded slower but more persistently, consistent with their increased cell translocation rates. Actin networks in Ena/VASP-deficient lamellipodia contained shorter, more highly branched filaments compared to controls. Lamellipodia with excess Ena/VASP contained longer, less branched filaments. In vitro, Ena/VASP promoted actin filament elongation by interacting with barbed ends, shielding them from capping protein. We conclude that Ena/VASP regulates cell motility by controlling the geometry of actin filament networks within lamellipodia. |
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