Nearly six decades ago, Lewis Wolpert proposed the relaxation of the polar cell cortex by the radial arrays of astral microtubules as a mechanism for cleavage furrow induction. While this mechanism has remained controversial, recent work has provided evidence for polar relaxation by astral microtubules, although its molecular mechanisms remain elusive. Here, using C. elegans embryos, we show that polar relaxation is achieved through dynein-mediated removal of myosin II from the polar cortexes. Mutants that position centrosomes closer to the polar cortex accelerated furrow induction, whereas suppression of dynein activity delayed furrowing. We show that dynein-mediated removal of myosin II from the polar cortexes triggers a bidirectional cortical flow toward the cell equator, which induces the assembly of the actomyosin contractile ring. These results provide a molecular mechanism for the aster-dependent polar relaxation, which works in parallel with equatorial stimulation to promote robust cytokinesis.

中文翻译：

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动力蛋白介导的皮质肌球蛋白 II 去除导致极性松弛

大约六十年前，刘易斯·沃尔珀特 (Lewis Wolpert) 提出，星体微管的径向阵列可以松弛极细胞皮层，作为卵裂沟诱导的机制。虽然这种机制仍然存在争议，但最近的工作为星体微管的极性弛豫提供了证据，尽管其分子机制仍然难以捉摸。在这里，我们使用线虫胚胎，证明极弛豫是通过动力蛋白介导的从极皮层去除肌球蛋白 II 来实现的。将中心体定位得更靠近极皮层的突变体加速了皱纹的诱导，而抑制动力蛋白活性则延迟了皱纹的产生。我们发现，动力蛋白介导的肌球蛋白 II 从极皮质的去除会触发皮质向细胞赤道的双向流动，从而诱导肌动球蛋白收缩环的组装。这些结果为紫苑依赖性极性弛豫提供了分子机制，该机制与赤道刺激并行作用，以促进强有力的胞质分裂。