Apical constriction (AC) is a widely utilized mechanism of cell shape change whereby epithelial cells transform from a cylindrical to conical shape, which can facilitate morphogenetic movements during embryonic development. Invertebrate epithelial cells undergoing AC depend on the contraction of apical cortex-spanning actomyosin filaments that generate force on the apical junctions and pull them toward the middle of the cell, effectively reducing the apical circumference. A current challenge is to determine whether these mechanisms are conserved in vertebrates and to identify the molecules responsible for linking apical junctions with the AC machinery. Utilizing the developing mouse eye as a model, we have uncovered evidence that lens placode AC may be partially dependent on apically positioned myosin-containing filaments associated with the zonula adherens. In addition we found that, among several junctional components, p120-catenin genetically interacts with Shroom3, a protein required for AC during embryonic morphogenesis. Further analysis revealed that, similar to Shroom3, p120-catenin is required for AC of lens cells. Finally, we determined that p120-catenin functions by recruiting Shroom3 to adherens junctions. Together, these data identify a novel role for p120-catenin during AC and further define the mechanisms required for vertebrate AC.

Development of the ocular lens commences with the formation of the lens placode, an epithelial structure that thickens and subsequently bends inward in a process called invagination. Invagination is observed during the development of many embryonic structures, but the spectrum of morphogenetic events driving this process are, in most cases, not fully understood. A characteristic commonly found in embryonic tissues undergoing epithelial reorganization is planar polarity, a property where cells are geometrically and/or molecularly orientated in a specific direction along the plane of an epithelium. Planar polarity is known to drive the morphogenesis of several epithelial structures, however its role during invagination events is less clear. We have found that at the onset of invagination, cells of the lens placode become geometrically planar polarized such that they are orientated toward a central point in the lens placode. Further investigation revealed that this is due to contraction of radially orientated junctions and the elongation of those circumferentially orientated. Radial junctions have an elevated localization of actomyosin and their contraction is dependent on the F-actin and Rho-kinase binding protein, Shroom3. Elongation of circumferential junctions is dependent upon Cdc42, a Rho-GTPase known to regulate polarity via the Par-complex. We determined that Cdc42 and members of the Par-complex inhibit Shroom3-induced contractility and promote anisotropic placode cell geometry through inhibition of junctional contraction. We postulate that invagination of the lens placode requires careful orchestration of these opposing processes which are mediated by the planar polarization of junctional proteins.