Centrosomes must resist microtubule-mediated forces for mitotic chromosome segregation. During mitotic exit, however, centrosomes are deformed and fractured by those same forces, which is a key step in centrosome disassembly. How the functional material properties of centrosomes change throughout the cell cycle, and how they are molecularly tuned, remain unknown. Here, we used optically induced flow perturbations to determine the molecular basis of centrosome strength and ductility in C. elegans embryos. We found that both properties declined sharply at anaphase onset, long before natural disassembly. This mechanical transition required PP2A phosphatase and correlated with inactivation of PLK-1 (Polo kinase) and SPD-2 (Cep192). In vitro, PLK-1 and SPD-2 directly protected centrosome scaffolds from force-induced disassembly. Our results suggest that, before anaphase, PLK-1 and SPD-2 respectively confer strength and ductility to the centrosome scaffold so that it can resist microtubule-pulling forces. In anaphase, centrosomes lose PLK-1 and SPD-2 and transition to a weak, brittle state that enables force-mediated centrosome disassembly.

中文翻译：

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有丝分裂退出过程中材料特性的调节变化是中心体解体的基础

中心体必须抵抗微管介导的有丝分裂染色体分离力。然而，在有丝分裂退出期间，中心体在这些相同的力的作用下变形和断裂，这是中心体解体的关键步骤。中心体的功能材料特性在整个细胞周期中如何变化，以及它们如何进行分子调节，仍然未知。在这里，我们使用光诱导流扰动来确定线虫胚胎中心体强度和延展性的分子基础。我们发现，早在自然分解之前，这两种特性就在后期开始时急剧下降。这种机械转变需要 PP2A 磷酸酶，并与 PLK-1（Polo 激酶）和 SPD-2（Cep192）的失活相关。在体外，PLK-1 和 SPD-2 直接保护中心体支架免受力诱导的分解。我们的结果表明，在后期之前，PLK-1 和 SPD-2 分别赋予中心体支架强度和延展性，使其能够抵抗微管拉力。在后期，中心体失去 PLK-1 和 SPD-2，并转变为弱而脆的状态，从而实现力介导的中心体解体。