Axons are living systems that display highly dynamic changes in stiffness, viscosity, and internal stress. However, the mechanistic origin of these phenomenological properties remains elusive. Here we establish a computational mechanics model that interprets cellular-level characteristics as emergent properties from molecular-level events. We create an axon model of discrete microtubules, which are connected to neighboring microtubules via discrete crosslinking mechanisms that obey a set of simple rules. We explore two types of mechanisms: passive and active crosslinking. Our passive and active simulations suggest that the stiffness and viscosity of the axon increase linearly with the crosslink density, and that both are highly sensitive to the crosslink detachment and reattachment times. Our model explains how active crosslinking with dynein motors generates internal stresses and actively drives axon elongation. We anticipate that our model will allow us to probe a wide variety of molecular phenomena—both in isolation and in interaction—to explore emergent cellular-level features under physiological and pathological conditions.

中文翻译：

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模拟轴突中的分子机制

轴突是生命系统，在刚度、粘度和内应力方面表现出高度动态的变化。然而，这些现象学特性的机械起源仍然难以捉摸。在这里，我们建立了一个计算力学模型，该模型将细胞水平的特征解释为分子水平事件的紧急特性。我们创建了离散微管的轴突模型，这些微管通过遵守一组简单规则的离散交联机制连接到相邻的微管。我们探索两种类型的机制：被动和主动交联。我们的被动和主动模拟表明，轴突的刚度和粘度随交联密度线性增加，并且两者都对交联脱离和重新附着时间高度敏感。我们的模型解释了与动力蛋白马达的主动交联如何产生内应力并主动驱动轴突伸长。我们预计我们的模型将使我们能够探索各种各样的分子现象——无论是孤立的还是相互作用的——以探索生理和病理条件下出现的细胞水平特征。