Wiesner Sebastian, Helfer Emmanuele, Didry Dominique, Ducouret Guylaine, Lafuma Françoise, Carlier Marie-France, Pantaloni Dominique
Dynamique du cytosquelette, Laboratoire d'Enzymologie et Biochimie Structurales, Centre National de la Recherche Scientifique, 91198 Gif-sur-Yvette, France.
J Cell Biol. 2003 Feb 3;160(3):387-98. doi: 10.1083/jcb.200207148. Epub 2003 Jan 27.
Abiomimetic motility assay is used to analyze the mechanism of force production by site-directed polymerization of actin. Polystyrene microspheres, functionalized in a controlled fashion by the N-WASP protein, the ubiquitous activator of Arp2/3 complex, undergo actin-based propulsion in a medium that consists of five pure proteins. We have analyzed the dependence of velocity on N-WASP surface density, on the concentration of capping protein, and on external force. Movement was not slowed down by increasing the diameter of the beads (0.2 to 3 microm) nor by increasing the viscosity of the medium by 10(5)-fold. This important result shows that forces due to actin polymerization are balanced by internal forces due to transient attachment of filament ends at the surface. These forces are greater than the viscous drag. Using Alexa488-labeled Arp2/3, we show that Arp2/3 is incorporated in the actin tail like G-actin by barbed end branching of filaments at the bead surface, not by side branching, and that filaments are more densely branched upon increasing gelsolin concentration. These data support models in which the rates of filament branching and capping control velocity, and autocatalytic branching of filament ends, rather than filament nucleation, occurs at the particle surface.
一种仿生运动分析方法被用于分析通过肌动蛋白的定点聚合产生力的机制。聚苯乙烯微球通过N-WASP蛋白(Arp2/3复合物的普遍激活剂)以可控方式进行功能化,在由五种纯蛋白组成的介质中经历基于肌动蛋白的推进。我们分析了速度对N-WASP表面密度、封端蛋白浓度和外力的依赖性。增加珠子直径(0.2至3微米)或使介质粘度增加10^5倍都不会使运动减慢。这一重要结果表明,肌动蛋白聚合产生的力被由于细丝末端在表面的瞬时附着产生的内力所平衡。这些力大于粘性阻力。使用Alexa488标记的Arp2/3,我们表明Arp2/3通过细丝在珠子表面的刺端分支而非侧分支并入肌动蛋白尾部,并且随着凝溶胶蛋白浓度的增加,细丝分支更密集。这些数据支持了这样的模型,即细丝分支和封端的速率控制速度,并且细丝末端的自催化分支而非细丝成核发生在颗粒表面。