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Drosophila p120catenin plays a supporting role in cell adhesion but is not an essential adherens junction component

机译:果蝇p120catenin在细胞粘附中起辅助作用,但不是必需的粘附连接成分

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Cadherin–catenin complexes, localized to adherens junctions, are essential for cell–cell adhesion. One means of regulating adhesion is through the juxtamembrane domain of the cadherin cytoplasmic tail. This region is the binding site for p120, leading to the hypothesis that p120 is a key regulator of cell adhesion. p120 has also been suggested to regulate the GTPase Rho and to regulate transcription via its binding partner Kaiso. To test these hypothesized functions, we turned to Drosophila, which has only a single p120 family member. It localizes to adherens junctions and binds the juxtamembrane region of DE-cadherin (DE-cad). We generated null alleles of p120 and found that mutants are viable and fertile and have no substantial changes in junction structure or function. However, p120 mutations strongly enhance mutations in the genes encoding DE-cadherin or Armadillo, the β-catenin homologue. Finally, we examined the localization of p120 during embryogenesis. p120 localizes to adherens junctions, but its localization there is less universal than that of core adherens junction proteins. Together, these data suggest that p120 is an important positive modulator of adhesion but that it is not an essential core component of adherens junctions.
机译:钙黏着蛋白-连环蛋白复合物位于粘附连接处,对细胞间粘附至关重要。调节粘附的一种方法是通过钙黏着蛋白胞质尾部的近膜结构域。该区域是p120的结合位点,从而导致以下假设:p120是细胞粘附的关键调节剂。还已经建议p120调节GTPase Rho并通过其结合伴侣Kaiso调节转录。为了测试这些假设的功能,我们求助于果蝇,果蝇只有一个p120家族成员。它定位于粘附连接并结合DE-钙粘蛋白(DE-cad)的近膜区域。我们产生了p120的无效等位基因,发现突变体是活的和可育的,并且在连接结构或功能上没有实质性的改变。然而,p120突变强烈增强了编码DE-钙粘蛋白或犰狳(β-catenin同源物)的基因中的突变。最后,我们检查了胚胎发生过程中p120的定位。 p120定位于粘附连接,但是其定位比核心粘附连接蛋白普遍。总之,这些数据表明p120是粘附的重要正调节剂,但它不是粘附连接的必不可少的核心成分。

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