Lindemann C B
Department of Biological Sciences, Oakland University, Rochester, Michigan.
Cell Motil Cytoskeleton. 1994;29(2):141-54. doi: 10.1002/cm.970290206.
Ciliary and flagellar motion is driven by the dynein-tubulin interaction between adjacent doublets of the axoneme, and the resulting sliding displacements are converted into axonemal bends that are propagated. When the axoneme is bent in the normal beating plane, force develops across the axoneme in the plane of the bend. This transverse force (t-force) has maximal effect on the interdoublet spacing of outer doublets 2-4 on one side of the axoneme and doublets 7-9 on the opposite side. Episodes of sliding originates as the t-force brings these doublets into closer proximity (allowing dynein bridges to form) and are terminated when these doublets are separated from each other by the t-force. A second factor, the adhesive force of the dynein-tubulin attachments (bridges), also acts to pull neighboring doublets closer together. This force resists termination of a sliding episode once initiated, and acts locally to give the population of dynein bridges a type of excitability. In other words, as bridges form, the probability of nearby bridges attaching is increased by a positive feedback exerted through the interdoublet spacing. A conceptual working hypothesis explaining the behavior of cilia and flagella is proposed based on the above concepts. Additionally, the feasibility of this proposed mechanism is demonstrated using a computer simulation. The simulation uses a Monte Carlo-type algorithm for dynein attachment and adhesive force, together with a geometric evaluation of the t-force on the key microtubule pairs. This model successfully develops spontaneous oscillations from any starting configuration (including a straight position). It is compatible with the physical dimensions, mechanical properties and bridge forces measured in real cilia and flagella. In operation, it exhibits many of the observed actions of cilia and flagella, most notably wave propagation and the ability to produce both cilia-like and flagella-like waveforms.
纤毛和鞭毛的运动是由轴丝相邻二联体之间的动力蛋白-微管蛋白相互作用驱动的，由此产生的滑动位移被转化为传播的轴丝弯曲。当轴丝在正常摆动平面内弯曲时，在弯曲平面内会在轴丝上产生力。这种横向力（t力）对轴丝一侧的外二联体2-4和另一侧的二联体7-9的二联体间距有最大影响。滑动事件的发生是由于t力使这些二联体靠得更近（允许形成动力蛋白桥），而当这些二联体被t力彼此分开时滑动事件终止。第二个因素，动力蛋白-微管蛋白附着（桥）的粘附力，也起到将相邻二联体拉得更近的作用。一旦启动，这种力会阻止滑动事件的终止，并在局部起作用，赋予动力蛋白桥群体一种兴奋性。换句话说，随着桥的形成，通过二联体间距施加的正反馈会增加附近桥附着的概率。基于上述概念，提出了一个解释纤毛和鞭毛行为的概念性工作假设。此外，使用计算机模拟证明了该提出机制的可行性。该模拟使用蒙特卡洛类型的算法来模拟动力蛋白附着和粘附力，同时对关键微管对的t力进行几何评估。该模型成功地从任何起始构型（包括直线位置）产生自发振荡。它与在真实纤毛和鞭毛中测量的物理尺寸、机械性能和桥力兼容。在运行中，它表现出许多观察到的纤毛和鞭毛的行为，最显著的是波传播以及产生纤毛样和鞭毛样波形的能力。
