Cell polarization enables zygotes to acquire spatial asymmetry, which in turn patterns cellular and tissue axes during development. Local modification in the actomyosin cytoskeleton mediates spatial segregation of partitioning-defective (PAR) proteins at the cortex, but how mechanical changes in the cytoskeleton are transmitted to PAR proteins remains elusive. Here we uncover a role of actomyosin contractility in the remodelling of PAR proteins through cortical clustering. During embryonic polarization in Caenorhabditis elegans, actomyosin contractility and the resultant cortical tension stimulate clustering of PAR-3 at the cortex. Clustering of atypical protein kinase C (aPKC) is supported by PAR-3 clusters and is antagonized by activation of CDC-42. Cortical clustering is associated with retardation of PAR protein exchange at the cortex and with effective entrainment of advective cortical flows. Our findings delineate how cytoskeleton contractility couples the cortical clustering and long-range displacement of PAR proteins during polarization. The principles described here would apply to other pattern formation processes that rely on local modification of cortical actomyosin and PAR proteins.

中文翻译：

---

皮质力和CDC-42控制线粒体秀丽隐杆线虫胚胎极化的PAR蛋白聚集。

细胞极化使受精卵获得空间不对称性，从而在发育过程中改变细胞和组织轴的模式。放线菌素细胞骨架的局部修饰介导了皮层中分区缺陷（PAR）蛋白质的空间分离，但是如何将细胞骨架的机械变化传递给PAR蛋白仍然不清楚。在这里，我们揭示了肌动球蛋白的收缩性在通过皮层聚簇的PAR蛋白重塑中的作用。在秀丽隐杆线虫的胚胎极化过程中，肌动球蛋白的收缩力和由此产生的皮质张力刺激了PAR-3在皮质的聚集。非典型蛋白激酶C（aPKC）的群集受PAR-3群集的支持，并因CDC-42的激活而被拮抗。皮质聚集与皮质中PAR蛋白交换的阻滞和对流皮质流的有效夹带有关。我们的发现描述了极化过程中细胞骨架的收缩力如何耦合皮层聚集和PAR蛋白的远距离移位。此处描述的原理将适用于依赖于皮质放线菌肌球蛋白和PAR蛋白的局部修饰的其他模式形成过程。