±-Catenin and IQGAP Regulate Myosin Localization to Control Epithelial Tube Morphogenesis in Dictyostelium

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 nonmetazoan 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 ±- and ²-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. º Apical actomyosin regulates morphology and luminal volume of a tubular epithelium º Apical contractility is a conserved morphogenetic mechanism in amoebozoa and animals º IQGAP1 promotes apical contractility by excluding myosin from the basolateral cortex º IQGAP1 acts downstream of epithelial polarity and is regulated by ²- and ±-catenin Formation of a tubular epithelium is essential for fruiting body morphogenesis in Dictyostelium. Dickinson et al. show that apical actomyosin contractility is required to organize this epithelial tube. An IQGAP1 complex acts downstream of ²- and ±-catenin to exclude myosin from the basolateral cortex, thereby promoting apical myosin enrichment.