A fundamental challenge in cell biology is to understand how cells generate actomyosin‐based contractile force. Here we study the actomyosin contractile ring that divides cells during cytokinesis and generates tension by a mechanism that remains poorly understood. Long ago a muscle‐like sliding filament mechanism was proposed, but evidence for sarcomeric organization in contractile rings is lacking. We develop a coarse‐grained model of the fission yeast cytokinetic ring, incorporating the two myosin‐II isoforms Myo2 and Myp2 and severely constrained by experimental data. The model predicts that ring tension is indeed generated by a sliding filament mechanism, but a spatially and temporally homogeneous version of that in muscle. In this mechanism all pairs of oppositely oriented actin filaments are rendered tense as they are pulled toward one another and slide through clusters of myosin‐II. The mechanism relies on anchoring of actin filament barbed ends to the plasma membrane, which resists lateral motion and enables filaments to become tense when pulled by myosin‐II. A second fixed filament component is independent of lateral anchoring, generated by chains of like‐oriented actin filaments. Myo2 contributes to both components, while Myp2 contributes to the sliding filament component only. In the face of instabilities inherent to actomyosin contractility, organizational homeostasis is maintained by rapid turnover of Myo2 and Myp2, and by drag forces that resist lateral motion of actin, Myo2 and Myp2. Thus, sliding and fixed filament mechanisms contribute to tension in the disordered contractile ring without the need for the sarcomeric architecture of muscle.

中文翻译：

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滑动细丝和固定细丝机制有助于细胞因子收缩环中的环张力。

细胞生物学的一个基本挑战是了解细胞如何产生基于肌动球蛋白的收缩力。在这里，我们研究了肌动球蛋白收缩环，它在胞质分裂过程中分裂细胞并通过一种仍然知之甚少的机制产生张力。很久以前就提出了一种类似肌肉的滑动细丝机制，但缺乏收缩环中肌节组织的证据。我们开发了裂殖酵母细胞因子环的粗粒度模型，结合了两种肌球蛋白 II 亚型 Myo2 和 Myp2，并受到实验数据的严重限制。该模型预测，环张力确实是由滑动细丝机制产生的，但在空间和时间上是肌肉中均匀的版本。在这种机制中，所有成对相反方向的肌动蛋白丝在被拉向彼此并滑过肌球蛋白 II 簇时都会变得紧张。该机制依赖于肌动蛋白丝带倒刺末端锚定在质膜上，从而抵抗横向运动并使细丝在被肌球蛋白 II 拉动时变得紧张。第二个固定的细丝成分独立于横向锚定，由相同取向的肌动蛋白细丝链产生。Myo2 对这两个组件都有贡献，而 Myp2 仅对滑动细丝组件有贡献。面对肌动球蛋白收缩固有的不稳定性，组织稳态通过 Myo2 和 Myp2 的快速周转以及抵抗肌动蛋白、Myo2 和 Myp2 横向运动的阻力来维持。因此，