Embryonic morphogenesis relies on the intrinsic ability of cells, often through remodeling the cytoskeleton, to shape epithelial tissues during development. Epithelial invagination is an example of morphogenesis that depends on this remodeling but the cellular mechanisms driving arrangement of cytoskeletal elements needed for tissue deformation remain incompletely characterized. To elucidate these mechanisms, live fluorescent microscopy and immunohistochemistry on fixed specimens were performed on chick and mouse lens placodes. This analysis revealed the formation of peripherally localized, circumferentially orientated and aligned junctions enriched in F-actin and MyoIIB. Once formed, the aligned junctions contract in a Rho-kinase and non-muscle myosin dependent manner. Further molecular characterization of these junctions revealed a Rho-kinase dependent accumulation of Arhgef11, a RhoA-specific guanine exchange factor known to regulate the formation of actomyosin cables and junctional contraction. In contrast, the localization of the Par-complex protein Par3, was reduced in these circumferentially orientated junctions. In an effort to determine if Par3 plays a negative role in MyoIIB accumulation, Par3-deficient mouse embryos were analyzed which not only revealed an increase in bicellular junctional accumulation of MyoIIB, but also a reduction of Arhgef11. Together, these results highlight the importance of the formation of the multicellular actomyosin cables that appear essential to the initiation of epithelial invagination and implicate the potential role of Arhgef11 and Par3 in their contraction and formation.
Keywords: Actomyosin; Actomyosin cable; Anisotropy; Arhgef11; Invagination; Lens placode; Morphogenesis; Nonmuscle myosin; PDZRhoGEF; Par3; Planar polarity; Pseudo sarcomeric filament; Rho-kinase; pard3.
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