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.

中文翻译：

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分子马达增强微管晶格可塑性

微管是活细胞的关键结构元素，对细胞分裂、细胞内运输和运动至关重要。最近的实验表明，微管切断蛋白和分子马达刺激游离微管蛋白直接和局部结合到轴中。然而，完全缺失微管相关蛋白如何影响晶格的机制图。在这里，我们从理论上探讨了由进行性分子马达刺激的晶格转换的潜在机制，其中马达步进对晶格的弱瞬态失稳促进了移动空位的形成。在没有游离微管蛋白的情况下，缺陷会迅速传播，导致完全骨折。在游离微管蛋白存在的情况下，运动行走会引起与运动行走相反方向的空位漂移。漂移伴随着沿着空位轨迹直接和局部掺入游离微管蛋白。我们的结果与实验一致，并强烈表明弱晶格 - 运动相互作用是增强微管轴可塑性的原因。