论文标题
分子电动机增强微管晶格可塑性
Molecular motors enhance microtubule lattice plasticity
论文作者
论文摘要
微管是活细胞的关键结构元素，这些元素对于细胞分裂，细胞内转运和运动性至关重要。最近的实验表明，微管断开蛋白质和分子电机会刺激游离小管蛋白直接和局部掺入到轴上。但是，机械图片如何完全缺少微管相关蛋白影响晶格。在这里，我们从理论上探索了通过加工分子电动机刺激的晶格周转的潜在机制，在该分子电机中，通过电动机踩踏的晶格较弱的瞬态不稳定可促进移动空缺的形成。在没有游离小管蛋白的情况下，缺陷迅速传播导致完全骨折。在存在游离小管蛋白的情况下，运动步行会引起空缺沿与运动步行相反的方向漂移。漂移伴随着自由小管蛋白沿空位的轨迹的直接和局部掺入。我们的结果与实验一致，并强烈表明弱晶格运动相互作用是造成增强的微管轴可塑性的原因。
Microtubules are key structural elements of living cells that are crucial for cell division, intracellular transport and motility. Recent experiments have shown that microtubule severing proteins and molecular motors stimulate the direct and localized incorporation of free tubulin into the shaft. However, a mechanistic picture how microtubule associated proteins affect the lattice is completely missing. Here we theoretically explore a potential mechanism of lattice turnover stimulated by processive molecular motors in which a weak transient destabilization of the lattice by the motor stepping promotes the formation of mobile vacancies. In the absence of free tubulin the defect rapidly propagates leading to a complete fracture. In the presence of free tubulin, the motor walk induces a vacancy drift in the direction opposite of the motor walk. The drift is accompanied by the direct and localized incorporation of free tubulin along the trajectory of the vacancy. Our results are consistent with experiments and strongly suggest that a weak lattice-motor interaction is responsible for an augmented microtubule shaft plasticity.
