Abstract
Adhesion molecules hold cells together but also couple cell membranes to a contractile actomyosin network, which limits the expansion of cell contacts. Despite their fundamental role in tissue morphogenesis and tissue homeostasis, how adhesion molecules control cell shapes and cell patterns in tissues remains unclear. Here we address this question in vivo using the Drosophila eye. We show that cone cell shapes depend little on adhesion bonds and mostly on contractile forces. However, N-cadherin has an indirect control on cell shape. At homotypic contacts, junctional N-cadherin bonds downregulate Myosin-II contractility. At heterotypic contacts with E-cadherin, unbound N-cadherin induces an asymmetric accumulation of Myosin-II, which leads to a highly contractile cell interface. Such differential regulation of contractility is essential for morphogenesis as loss of N-cadherin disrupts cell rearrangements. Our results establish a quantitative link between adhesion and contractility and reveal an unprecedented role of N-cadherin on cell shapes and cell arrangements.
Highlights
Cells acquire different shapes and arrangements to form tissues, depending on their functions and microenvironment
Cell Biology Developmental Biology and Stem Cells actomyosin contractility? To address these questions, we investigated the origin of cell shapes in vivo in the highly organized Drosophila retina, which features differential expression of cadherin molecules and is amenable to quantification of cell shapes and mechanical measurements
We showed that the adhesion provided by Ecad and Ncad homophilic bonds have a moderate direct contribution to interfacial tension as compared to MyoII dependent contractile forces
Summary
Cells acquire different shapes and arrangements to form tissues, depending on their functions and microenvironment. Cells actively form and remodel their cell contacts, generating forces to drive various morphogenetic events (Lecuit and Lenne, 2007). Two systems contribute to changes in cell contacts: Cadherin complexes and actomyosin networks (Harris, 2012; Baum and Georgiou, 2011). Actomyosin contractility acts antagonistically by reducing cell contact size (Lecuit and Lenne, 2007; Winklbauer, 2015). In Drosophila retina, N-cadherin mutants show drastic alteration of contact size and cell shape (Hayashi and Carthew, 2004), which suggests that cadherin-associated adhesion cannot be discounted. Even though the forces produced by cadherins and actomyosin networks act antagonistically, both systems are interconnected as cadherins are associated with intracellular actomyosin networks via catenins and other actin-binding proteins (Priya et al, 2013; Roper, 2015)
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