Myosin and kinesin are biomolecular motors found in living cells. By propelling their associated cytoskeletal filaments, these biomolecular motors facilitate force generation and material transport in the cells. When extracted, the biomolecular motors are promising candidates for in vitro applications such as biosensor devices, on account of their high operating efficiency and nanoscale size. However, during integration into these devices, some of the motors become defective due to unfavorable adhesion to the substrate surface. These defective motors inhibit the motility of the cytoskeletal filaments which make up the molecular shuttles used in the devices. Difficulties in controlling the fraction of active and defective motors in experiments discourage systematic studies concerning the resilience of the molecular shuttle motility against the impedance of defective motors. Here, we used mathematical modelling to systematically examine the resilience of the propulsion by these molecular shuttles against the impedance of the defective motors. The model showed that the fraction of active motors on the substrate is the essential factor determining the resilience of the molecular shuttle motility. Approximately 40% of active kinesin or 80% of active myosin motors are required to constitute continuous gliding of molecular shuttles in their respective substrates. The simplicity of the mathematical model in describing motility behavior offers utility in elucidating the mechanisms of the motility resilience of molecular shuttles.

中文翻译：

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分子梭针对有缺陷的马达的运动弹性


肌球蛋白和驱动蛋白是活细胞中发现的生物分子马达。通过推动相关的细胞骨架丝，这些生物分子马达促进细胞中力的产生和物质运输。当提取时，生物分子马达由于其高运行效率和纳米级尺寸而成为生物传感器设备等体外应用的有希望的候选者。然而，在集成到这些设备中时，一些电机由于与基板表面的粘合不良而出现缺陷。这些有缺陷的马达抑制了细胞骨架丝的运动性，而细胞骨架丝构成了设备中使用的分子穿梭机。实验中控制活性电机和缺陷电机比例的困难阻碍了关于分子梭运动对抗缺陷电机阻抗的弹性的系统研究。在这里，我们使用数学模型来系统地检查这些分子梭的推进力相对于有缺陷的电机的阻抗的弹性。该模型表明，基底上主动马达的比例是决定分子穿梭运动弹性的重要因素。需要大约 40% 的活性驱动蛋白或 80% 的活性肌球蛋白马达来构成分子穿梭机在其各自基质中的连续滑行。描述运动行为的数学模型的简单性为阐明分子穿梭运动弹性的机制提供了实用性。