NOVEL FORM OF GROWTH CONE MOTILITY INVOLVING SITE-DIRECTED ACTIN FILAMENT ASSEMBLY
NOVEL FORM OF GROWTH CONE MOTILITY INVOLVING SITE-DIRECTED ACTIN FILAMENT ASSEMBLY
复制标题
DOI：
10.1038/357515a0
复制
发表时间：
1992-06-11
期刊：
影响因子：
64.8
通讯作者：
THOMPSON, C
中科院分区：
文献类型：
--
作者：
FORSCHER, P;LIN, CH;THOMPSON, C
细胞外信号对细胞骨架结构和运动性的调节对于所有定向形式的细胞运动都是必不可少的，并且是神经元生长锥中轴突导向发育过程的基础。与多阳离子微珠的相互作用可以引发神经元和肌肉细胞的形态发生变化，这些变化通常与突触前和突触后特化结构的形成有关[1,2]。此外，当各种类型的微小颗粒应用于神经元生长锥或运动细胞的片状表面时，它们常常以1 - 6μm/min的速度呈现逆行运动（参考文献3 - 6）。有强有力的证据表明，这种形式的颗粒运动是由与皮质F - 肌动蛋白网络相关的膜蛋白易位引起的，而不是由大量的逆行脂质流动引起的[4,5,7]，并且可能是细胞移动、生长锥迁移和细胞表面抗原成帽等过程背后的一种机制[6,8,9]。在这里我们报道一种由多阳离子微珠与生长锥膜表面相互作用所刺激的新的运动形式。微珠结合迅速诱导细胞内肌动蛋白丝组装，同时产生足以驱动微珠运动的力。这些细胞外微珠运动类似于已知的细菌寄生虫的细胞内运动，细菌寄生虫通过重定向宿主细胞F - 肌动蛋白组装来推进自身。我们的结果表明，定点的肌动蛋白丝组装可能是一种在膜 - 细胞骨架界面产生力的广泛的细胞机制。
REGULATION of cytoskeletal structure and motility by extracellular signals is essential for all directed forms of cell movement and underlies the developmental process of axonal guidance in neuronal growth cones. Interaction with polycationic microbeads can trigger morphogenic changes in neurons and muscle cells normally associated with formation of pre- and postsynaptic specializations 1,2. Furthermore, when various types of microscopic particles are applied to the lamellar surface of a neuronal growth cone or motile cell they often exhibit retrograde movement at rates of 1-6-mu-m min-1 (refs 3-6). There is strong evidence that this form of particle movement results from translocation of membrane proteins associated with cortical F-actin networks, not from bulk retrograde lipid flow 4,5,7 and may be a mechanism behind processes such as cell locomotion, growth cone migration and capping of cell-surface antigens 6,8,9. Here we report a new form of motility stimulated by polycationic bead interactions with the growth-cone membrane surface. Bead binding rapidly induces intracellular actin filament assembly, coincident with a production of force sufficient to drive bead movements. These extracellular bead movements resemble intracellular movements of bacterial parasites known to redirect host cell F-actin assembly for propulsion. Our results suggest that site-directed actin filament assembly may be a widespread cellular mechanism for generating force at membrane-cytoskeletal interfaces.