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

Program in Cancer Biology, Stanford University, Stanford, CA 94305, USA.
Developmental Cell (Impact Factor: 9.71). 08/2012; 23(3):533-46. DOI: 10.1016/j.devcel.2012.06.008
Source: PubMed


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 α- and β-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.

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Available from: Douglas N Robinson, Oct 30, 2014
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    • "During PANC-1 cells stimulation, Rac1-GTP increases, binds IQGAP1 which dissociates from the E-cadherin complex inducing AJ destabilization [12]. In the culminant of the nonmetazoan Dictyostelium discoideum β- and α-catenin recruit IQGAP1 to lateral epithelial cell-cell contact but β- and α-catenin localization at cell-cell contact is independent of IQGAP1 [13]. In human ECs, IQGAP1 colocalized and interacts with VE-cadherin and β-catenin at sites of cell-cell contact and knockdown of IQGAP1 with siRNA inhibits the localization of VE-cadherin at AJ [8] and disrupts the endothelial barrier [14]. "
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