Department of Physics, Virginia Polytechnic Institute and State University, Blacksburg, Virginia.
Department of Biological Sciences, Virginia Polytechnic Institute and State University, Blacksburg, Virginia; Fralin Life Sciences Institute, Virginia Polytechnic Institute and State University, Blacksburg, Virginia.
Biophys J. 2022 Jun 21;121(12):2461-2473. doi: 10.1016/j.bpj.2022.05.012. Epub 2022 May 18.
Contrasting most known bacterial motility mechanisms, a bacterial sliding motility discovered in at least two gram-positive bacterial families does not depend on designated motors. Instead, the cells maintain end-to-end connections following cell divisions to form long chains and exploit cell growth and division to push the cells forward. To investigate the dynamics of this motility mechanism, we constructed a mechanical model that depicts the interplay of the forces acting on and between the cells comprising the chain. Due to the exponential growth of individual cells, the tips of the chains can, in principle, accelerate to speeds faster than any known single-cell motility mechanism can achieve. However, analysis of the mechanical model shows that the exponential acceleration comes at the cost of an exponential buildup in mechanical stress in the chain, making overly long chains prone to breakage. Additionally, the mechanical model reveals that the dynamics of the chain expansion hinges on a single non-dimensional parameter. Perturbation analysis of the mechanical model further predicts the critical stress leading to chain breakage and its dependence on the non-dimensional parameter. Finally, we developed a simplistic population-expansion model that uses the predicted breaking behavior to estimate the physical limit of chain-mediated population expansion. Predictions from the models provide critical insights into how this motility depends on key physical properties of the cell and the substrate. Overall, our models present a generically applicable theoretical framework for cell-chain-mediated bacterial sliding motility and provide guidance for future experimental studies on such motility.
与大多数已知的细菌运动机制相反,至少在两个革兰氏阳性菌家族中发现的细菌滑动运动不依赖于指定的马达。相反,细胞在细胞分裂后保持端到端的连接,形成长链,并利用细胞生长和分裂来推动细胞前进。为了研究这种运动机制的动力学,我们构建了一个力学模型,描绘了作用在链中包含的细胞上和细胞之间的力的相互作用。由于单个细胞的指数增长,原则上,链的尖端可以加速到比任何已知的单细胞运动机制都能达到的速度更快。然而,力学模型的分析表明,指数加速是以链中机械应力的指数积累为代价的,这使得过长的链容易断裂。此外,力学模型还揭示了链扩张的动力学取决于一个单一的无量纲参数。力学模型的摄动分析进一步预测了导致链断裂的临界应力及其对无量纲参数的依赖性。最后,我们开发了一个简单的群体扩张模型,该模型利用预测的断裂行为来估计链介导的群体扩张的物理极限。模型的预测提供了对这种运动如何依赖于细胞和基质的关键物理特性的重要见解。总的来说,我们的模型为细胞链介导的细菌滑动运动提供了一个通用的理论框架,并为未来关于这种运动的实验研究提供了指导。