During host infection, Toxoplasma gondii and related unicellular parasites move using gliding, which differs fundamentally from other known mechanisms of eukaryotic cell motility. Gliding is thought to be powered by a thin layer of flowing filamentous (F)-actin sandwiched between the plasma membrane and a myosin-covered inner membrane complex. How this surface actin layer drives the various gliding modes observed in experiments—helical, circular, twirling and patch, pendulum or rolling—is unclear. Here we suggest that F-actin flows arise through self-organization and develop a continuum model of emergent F-actin flow within the confines provided by Toxoplasma geometry. In the presence of F-actin turnover, our model predicts the emergence of a steady-state mode in which actin transport is largely directed rearward. Removing F-actin turnover leads to actin patches that recirculate up and down the cell, which we observe experimentally for drug-stabilized actin bundles in live Toxoplasma gondii parasites. These distinct self-organized actin states can account for observed gliding modes, illustrating how different forms of gliding motility can emerge as an intrinsic consequence of the self-organizing properties of F-actin flow in a confined geometry.

在宿主感染期间，弓形虫和相关的单细胞寄生虫使用滑动移动，这与其他已知的真核细胞运动机制有着根本的不同。滑行被认为由夹在质膜和肌球蛋白覆盖的内膜复合物之间的一层流动的丝状 （F）-肌动蛋白提供动力。该表面肌动蛋白层如何驱动实验中观察到的各种滑行模式（螺旋、圆形、旋转和贴片、钟摆或滚动）尚不清楚。在这里，我们建议 F-肌动蛋白流通过自组织产生，并在弓形虫几何学提供的范围内发展出苗 F-肌动蛋白流的连续体模型。在 F-肌动蛋白周转的情况下，我们的模型预测了一种稳态模式的出现，其中肌动蛋白运输主要向后引导。去除 F-肌动蛋白周转导致肌动蛋白斑块在细胞中上下再循环，我们在实验中观察活弓形虫寄生虫中药物稳定的肌动蛋白束。这些不同的自组织肌动蛋白状态可以解释观察到的滑行模式，说明了不同形式的滑行运动如何作为受限几何中 F-肌动蛋白流的自组织特性的内在结果出现。