To divide, bacteria must constrict their membranes against significant force from turgor pressure. A tubulin homolog, FtsZ, is thought to drive constriction, but how FtsZ filaments might generate constrictive force in the absence of motor proteins is not well understood. There are two predominant models in the field. In one, FtsZ filaments overlap to form complete rings around the circumference of the cell, and attractive forces cause filaments to slide past each other to maximize lateral contact. In the other, filaments exert force on the membrane by a GTP-hydrolysis-induced switch in conformation from straight to bent. Here, we developed software, ZCONSTRICT, for quantitative three-dimensional (3D) simulations of Gram-negative bacterial cell division to test these two models and identify critical conditions required for them to work. We find that the avidity of any kind of lateral interactions quickly halts the sliding of filaments, so a mechanism such as depolymerization or treadmilling is required to sustain constriction by filament sliding. For filament bending, we find that a mechanism such as the presence of a rigid linker is required to constrain bending to within the division plane and maintain the distance observed in vivo between the filaments and the membrane. Of these two models, only the filament bending model is consistent with our lab’s recent observation of constriction associated with a single, short FtsZ filament.

中文翻译：

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FtsZ驱动的细胞收缩机制的模拟

为了分裂，细菌必须收缩其膜以抵抗来自膨胀压力的巨大作用力。微管蛋白同系物FtsZ被认为可以驱动收缩，但是在缺乏运动蛋白的情况下，FtsZ细丝如何产生收缩力尚不十分清楚。该领域有两个主要模型。在一种情况下，FtsZ细丝重叠形成围绕电池圆周的完整环，并且吸引力使细丝彼此滑过以最大化横向接触。另一方面，细丝通过GTP水解诱导的开关以从笔直到弯曲的形式在膜上施加力。在这里，我们开发了ZCONSTRICT软件，用于革兰氏阴性细菌细胞分裂的定量三维（3D）模拟，以测试这两种模型并确定它们起作用所需的关键条件。我们发现，任何类型的横向相互作用的亲合力都会迅速停止长丝的滑动，因此需要一种解聚或踏车这样的机制来维持长丝滑动所产生的收缩。对于细丝弯曲，我们发现需要一种机制，例如存在刚性连接器，才能将弯曲限制在分隔平面内并保持观察到的距离丝和膜之间的体内。在这两个模型中，只有细丝弯曲模型与我们实验室最近观察到的与单根短FtsZ细丝相关的收缩一致。