A disassembly-driven mechanism explains F-actin-mediated chromosome transport in starfish oocytes
A disassembly-driven mechanism explains F-actin-mediated chromosome transport in starfish oocytes
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DOI：
10.7554/elife.31469
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发表时间：
2018-01-19
期刊：
影响因子：
7.7
通讯作者：
Lenart, Peter
中科院分区：
文献类型：
--
作者：
Bun, Philippe;Dmitrieff, Serge;Lenart, Peter
虽然肌节肌动球蛋白组件的收缩是很好的理解，这是不是肌动蛋白丝（F-肌动蛋白）驱动动物细胞中的各种基本过程的无序网络的情况。例如，在海星卵母细胞减数分裂开始时，在核区域形成收缩性F-肌动蛋白网络，将嵌入的染色体运送到组装微管纺锤体。在这里，我们通过比较定量观察和计算模型，解决了这种3D无序F-actin网络收缩的驱动机制。我们分析了3D染色体轨迹和成像细丝动力学，以监测各种物理和化学扰动下的网络行为。我们没有发现肌球蛋白活性驱动网络收缩的证据。相反，我们的观察结果很好地解释了基于解体驱动的收缩机制的模型。我们在计算机上重建了这种基于解体的收缩系统，揭示了一种简单的结构，该结构可以有力地驱动染色体运输，以防止大卵母细胞中的非整倍体，这是正常胚胎发育的先决条件。
While contraction of sarcomeric actomyosin assemblies is well understood, this is not the case for disordered networks of actin filaments (F-actin) driving diverse essential processes in animal cells. For example, at the onset of meiosis in starfish oocytes a contractile F-actin network forms in the nuclear region transporting embedded chromosomes to the assembling microtubule spindle. Here, we addressed the mechanism driving contraction of this 3D disordered F-actin network by comparing quantitative observations to computational models. We analyzed 3D chromosome trajectories and imaged filament dynamics to monitor network behavior under various physical and chemical perturbations. We found no evidence of myosin activity driving network contractility. Instead, our observations are well explained by models based on a disassembly-driven contractile mechanism. We reconstitute this disassembly-based contractile system in silico revealing a simple architecture that robustly drives chromosome transport to prevent aneuploidy in the large oocyte, a prerequisite for normal embryonic development.