论文标题
被动交联对肌动蛋白环的收缩
Constriction of actin rings by passive crosslinkers
论文作者
论文摘要
在许多生物体中，细胞分裂是由细胞动力环的收缩驱动的，细胞动力环由肌动蛋白丝和交联蛋白组成。尽管长期以来一直认为收缩是由运动蛋白驱动的，但最近已经发现，不移交燃料的被动交联链能够产生足够的力来收缩肌动蛋白丝环。为了研究环收缩动力学，我们开发了一个模型，其中包括交联凝结的驱动力以及摩擦和细丝弯曲的对立力。我们将收缩力分析为环拓扑和交联浓度的函数，并预测足以收缩未经修饰的质膜的力。我们的模型还预测，肌动蛋白丝滑动是由细丝旋转和交联之间的相互作用引起的，与交联链介导的微管滑动相比，摩擦力很低。
In many organisms, cell division is driven by the constriction of a cytokinetic ring, which consists of actin filaments and crosslinking proteins. While it has long been believed that the constriction is driven by motor proteins, it has recently been discovered that passive crosslinkers that do not turn over fuel are able to generate enough force to constrict actin filament rings. To study the ring constriction dynamics, we develop a model that includes the driving force of crosslinker condensation and the opposing forces of friction and filament bending. We analyze the constriction force as a function of ring topology and crosslinker concentration, and predict forces that are sufficient to constrict an unadorned plasma membrane. Our model also predicts that actin-filament sliding arises from an interplay between filament rotation and crosslinker hopping, producing frictional forces that are low compared to those of crosslinker-mediated microtubule sliding.
