Polarized epithelia develop distinct cell surface domains, with the apical membrane acquiring characteristic morphological features such as microvilli. Cell polarization is driven by polarity determinants including the evolutionarily conserved partitioning-defective (PAR) proteins that are separated into distinct cortical domains. PAR protein segregation is thought to be a consequence of asymmetric actomyosin contractions. The mechanism of activation of apically polarized actomyosin contractility is unknown. Here we show that the Cdc42 effector MRCK activates myosin-II at the apical pole to segregate aPKC–Par6 from junctional Par3, defining the apical domain. Apically polarized MRCK-activated actomyosin contractility is reinforced by cooperation with aPKC–Par6 downregulating antagonistic RhoA-driven junctional actomyosin contractility, and drives polarization of cytosolic brush border determinants and apical morphogenesis. MRCK-activated polarized actomyosin contractility is required for apical differentiation and morphogenesis in vertebrate epithelia and Drosophila photoreceptors. Our results identify an apical origin of actomyosin-driven morphogenesis that couples cytoskeletal reorganization to PAR polarity signalling.

中文翻译：

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顶端MRCK驱动的形态发生途径控制上皮极性

极化的上皮细胞形成独特的细胞表面结构域，其顶端膜具有特征性形态特征，例如微绒毛。细胞极化是由极性决定因素驱动的，这些决定因素包括进化上保守的分区缺陷（PAR）蛋白，该蛋白被分为不同的皮质结构域。PAR蛋白的分离被认为是肌动球蛋白不对称收缩的结果。顶极化的肌动球蛋白收缩性激活的机制尚不清楚。在这里，我们显示Cdc42效应器MRCK激活了顶端的肌球蛋白II，以将aPKC–Par6与连接的Par3分离，从而定义了顶端结构域。通过与aPKC-Par6下调拮抗RhoA驱动的连接性肌动球蛋白收缩力相结合，增强了两极极化的MRCK激活的肌动球蛋白收缩力，并驱动胞浆刷状边界决定簇的极化和根尖形态发生。脊椎动物上皮细胞的顶端分化和形态发生需要MRCK激活的极化肌动球蛋白收缩力。果蝇感光器。我们的研究结果确定了肌动球蛋白驱动的形态发生的根源，该形态发生将细胞骨架重组与PAR极性信号传导耦合在一起。