Eddy R J, Han J, Condeelis J S
Department of Anatomy and Structural Biology, Albert Einstein College of Medicine of Yeshiva University, Bronx, New York 10461, USA.
J Cell Biol. 1997 Dec 1;139(5):1243-53. doi: 10.1083/jcb.139.5.1243.
The first step in the directed movement of cells toward a chemotactic source involves the extension of pseudopods initiated by the focal nucleation and polymerization of actin at the leading edge of the cell. We have previously isolated a chemoattractant-regulated barbed-end capping activity from Dictyostelium that is uniquely associated with capping protein, also known as cap32/34. Although uncapping of barbed ends by capping protein has been proposed as a mechanism for the generation of free barbed ends after stimulation, in vitro and in situ analysis of the association of capping protein with the actin cytoskeleton after stimulation reveals that capping protein enters, but does not exit, the cytoskeleton during the initiation of actin polymerization. Increased association of capping protein with regions of the cell containing free barbed ends as visualized by exogenous rhodamine-labeled G-actin is also observed after stimulation. An approximate threefold increase in the number of filaments with free barbed ends is accompanied by increases in absolute filament number, whereas the average filament length remains constant. Therefore, a mechanism in which preexisting filaments are uncapped by capping protein, in response to stimulation leading to the generation of free barbed ends and filament elongation, is not supported. A model for actin assembly after stimulation, whereby free barbed ends are generated by either filament severing or de novo nucleation is proposed. In this model, exposure of free barbed ends results in actin assembly, followed by entry of free capping protein into the actin cytoskeleton, which acts to terminate, not initiate, the actin polymerization transient.
细胞向趋化源定向移动的第一步涉及伪足的延伸,这是由肌动蛋白在细胞前沿的局部成核和聚合引发的。我们之前从盘基网柄菌中分离出一种受趋化因子调节的带刺末端封端活性,它与封端蛋白(也称为cap32/34)独特相关。尽管有人提出封端蛋白解开带刺末端是刺激后产生游离带刺末端的一种机制,但刺激后对封端蛋白与肌动蛋白细胞骨架关联的体外和原位分析表明,在肌动蛋白聚合起始过程中,封端蛋白进入但未离开细胞骨架。刺激后还观察到,通过外源性罗丹明标记的G-肌动蛋白可视化显示,封端蛋白与含有游离带刺末端的细胞区域的关联增加。带有游离带刺末端的细丝数量大约增加了三倍,同时细丝的绝对数量也增加,而细丝的平均长度保持不变。因此,一种认为预先存在细丝被封端蛋白解开,以响应刺激导致游离带刺末端产生和细丝伸长的机制不成立。本文提出了一种刺激后肌动蛋白组装的模型,即游离带刺末端通过细丝切断或从头成核产生。在这个模型中,游离带刺末端的暴露导致肌动蛋白组装,随后游离封端蛋白进入肌动蛋白细胞骨架,其作用是终止而非启动肌动蛋白聚合瞬变。