α-Catenin and IQGAP Regulate Myosin Localization to Control Epithelial Tube Morphogenesis in Dictyostelium
α-Catenin and IQGAP Regulate Myosin Localization to Control Epithelial Tube Morphogenesis in Dictyostelium
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DOI：
10.1016/j.devcel.2012.06.008
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发表时间：
2012-09-11
影响因子：
11.8
通讯作者：
Weis, William I.
中科院分区：
文献类型：
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作者：
Dickinson, Daniel J.;Robinson, Douglas N.;Weis, William I.
动物上皮细胞的顶端肌动球蛋白活性影响组织形态并驱动发育过程中的形态发生运动。导致肌球蛋白II在根尖膜积聚并被其他膜排斥的分子机制尚不清楚。我们发现，在非后生动物盘状盘基骨柱中，肌凝蛋白II主要定位于围绕茎的顶端上皮细胞，而这种上皮管的收缩是正常形态发生所必需的。IQGAP1及其结合伙伴cortexillin I在α -和β -连环蛋白的下游发挥作用，将肌球蛋白II排除在基底外侧皮层之外，促进肌球蛋白II的顶端积累。IQGAP1或cortexillin的缺失损害上皮形态发生，但不影响细胞极性。这些结果揭示了肌球蛋白II的顶端定位是一个保守的形态发生机制，从非后生动物到脊椎动物，并确定了一个简单模式生物中调节上皮管极性和组织的蛋白层次。
Apical actomyosin activity in animal epithelial cells influences tissue morphology and drives morphogenetic movements during development. The molecular mechanisms leading to myosin II accumulation at the apical membrane and its exclusion from other membranes are poorly understood. We show that in the non metazoan Dictyostelium discoideum, myosin II localizes apically in tip epithelial cells that surround the stalk, and constriction of this epithelial tube is required for proper morphogenesis. IQGAP1 and its binding partner cortexillin I function downstream of alpha- and beta-catenin to exclude myosin II from the basolateral cortex and promote apical accumulation of myosin II. Deletion of IQGAP1 or cortexillin compromises epithelial morphogenesis without affecting cell polarity. These results reveal that apical localization of myosin II is a conserved morphogenetic mechanism from nonmetazoans to vertebrates and identify a hierarchy of proteins that regulate the polarity and organization of an epithelial tube in a simple model organism.