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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Reconstitution of the transition from lamellipodium to filopodium in a membrane-free system
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Reconstitution of the transition from lamellipodium to filopodium in a membrane-free system

机译：在无膜系统中重建lalamlipodium到filopodium的转变

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摘要

The cellular cytoskeleton is a complex dynamical network that constantly remodels as cells divide and move. This reorganization process occurs not only at the cell membrane, but also in the cell interior (bulk). During locomotion, regulated actin assembly near the plasma membrane produces lamellipodia and filopodia. Therefore, most in vitro experiments explore phenomena taking place in the vicinity of a surface. To understand how the molecular machinery of a cell self-organizes in a more general way, we studied bulk polymerization of actin in the presence of actin-related protein 2/3 complex and a nucleation promoting factor as a model for actin assembly in the cell interior separate from membranes. Bulk polymerization of actin in the presence of the verprolin homology, cofilin homology, and acidic region, domain of Wiskott-Aldrich syndrome protein, and actin-related protein 2/3 complex results in spontaneous formation of diffuse aster-like structures. In the presence of fascin these asters transition into stars with bundles of actin filaments growing from the surface, similar to star-like structures recently observed in vivo. The transition from asters to stars depends on the ratio [fascin]/[G actin]. The polarity of the actin filaments during the transition is preserved, as in the transition from lamellipodia to filopodia. Capping protein inhibits star formation. Based on these experiments and kinetic Monte Carlo simulations, we propose a model for the spontaneous self-assembly of asters and their transition into stars. This mechanism may apply to the transition from lamellipodia to filopodia in vivo.
机译：细胞的细胞骨架是一个复杂的动力学网络，随着细胞分裂和移动而不断地重塑。这种重组过程不仅发生在细胞膜上，而且发生在细胞内部（体）。在运动过程中，质膜附近的肌动蛋白组装受到调节，产生了片状脂蛋白缺乏和丝状伪足。因此，大多数体外实验探索在表面附近发生的现象。为了了解细胞的分子机制如何以更一般的方式自我组织，我们研究了肌动蛋白在存在肌动蛋白相关蛋白2/3复合物和成核促进因子作为细胞中肌动蛋白组装模型的条件下的本体聚合内部与膜分离。肌动蛋白在verprolin同源性，cofilin同源性和酸性区域，Wiskott-Aldrich综合征蛋白域和肌动蛋白相关蛋白2/3复合体的存在下发生本体聚合，导致自发形成分散的紫aster状结构。在存在fascin的情况下，这些紫苑会转变成具有从表面生长的肌动蛋白丝束的恒星，类似于最近在体内观察到的星形结构。从翠菊到恒星的转变取决于[fascin] / [G actin]的比率。过渡期间肌动蛋白丝的极性得以保留，就像从lamellipodia到filopodia的过渡一样。加帽的蛋白质抑制星的形成。基于这些实验和动力学蒙特卡洛模拟，我们提出了一个用于翠菊自发自组装及其向恒星过渡的模型。该机制可能适用于体内从片状脂蛋白到丝状伪足的过渡。

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