Author/Authors :
James E. Bear، نويسنده , , Tatyana M. Svitkina، نويسنده , , Matthias Krause، نويسنده , , Dorothy A. Schafer، نويسنده , , Joseph J. Loureiro، نويسنده , , Geraldine A. Strasser، نويسنده , , Ivan V. Maly، نويسنده , , Oleg Y. Chaga، نويسنده , , John A. Cooper، نويسنده , , Gary G. Borisy، نويسنده , , Frank B. Gertler، نويسنده ,
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.
