The planar cell polarity pathway regulates cell polarity, adhesion, and rearrangement. Its cytoplasmic core components Prickle (Pk) and Dishevelled (Dvl) often localize as dense puncta at cell membranes to form antagonizing complexes and establish cell asymmetry. In vertebrates, Pk and Dvl have been implicated in actomyosin cortex regulation, but the mechanism of how these proteins control cell mechanics is unclear. Here we demonstrate that in Xenopus prechordal mesoderm cells, diffusely distributed, cytoplasmic Pk1 up-regulates the F-actin content of the cortex. This counteracts cortex down-regulation by Dvl2. Both factors act upstream of casein kinase II to increase or decrease cortical tension. Thus, cortex modulation by Pk1 and Dvl2 is translated into mechanical force and affects cell migration and rearrangement during radial intercalation in the prechordal mesoderm. Pk1 also forms puncta and plaques, which are associated with localized depletion of cortical F-actin, suggesting opposite roles for diffuse and punctate Pk1.

中文翻译：

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平面细胞极性蛋白 Prickle1 对细胞皮层的调节


平面细胞极性途径调节细胞极性、粘附和重排。其细胞质核心成分 Prickle (Pk) 和 Disheveled (Dvl) 通常在细胞膜上形成致密的点，形成拮抗复合物并建立细胞不对称性。在脊椎动物中，Pk 和 Dvl 与肌动球蛋白皮质调节有关，但这些蛋白质如何控制细胞力学的机制尚不清楚。在这里，我们证明在爪蟾前脊索中胚层细胞中，弥漫分布的细胞质 Pk1 上调皮质的 F-肌动蛋白含量。这抵消了 Dvl2 对皮质的下调。这两个因子都作用于酪蛋白激酶 II 的上游，以增加或减少皮质张力。因此，Pk1 和 Dvl2 的皮层调节转化为机械力，并影响脊索前中胚层径向嵌入过程中的细胞迁移和重排。 Pk1 还形成点状和斑块，这与皮质 F-肌动蛋白的局部消耗有关，表明弥漫性和点状 Pk1 的作用相反。