arXivDaily arXiv每日学术速递 周一至周五更新
arXiv 2209.09161cond-mat.softq-bio.SC
收藏

分子马达增强微管晶格可塑性

Molecular motors enhance microtubule lattice plasticity

William Lecompte, Karin John

摘要:

微管是活细胞的关键结构元件,对于细胞分裂、细胞内运输和运动至关重要。最近的实验表明,微管切割蛋白和分子马达刺激游离微管蛋白直接和局部掺入到轴中。然而,微管相关蛋白如何影响晶格的机制图片是完全缺失的。在这里,我们从理论上探讨了一个潜在的机制,晶格周转的过程性分子马达刺激,其中一个弱的瞬态不稳定的晶格马达步进促进移动空位的形成。在没有游离微管蛋白的情况下,缺陷迅速扩展,导致完全断裂。在存在自由微管蛋白的情况下,马达行走诱导在与马达行走相反的方向上的空位漂移。漂移是伴随着直接和本地化的免费的微管蛋白的掺入沿轨迹的空缺。我们的研究结果与实验一致,并强烈表明,一个弱的晶格电机相互作用是负责增强微管轴可塑性。

英文摘要:

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.

机构、总结、中文摘要均由AI分析而来,可能存在错误,请以论文正文为准。

↑