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FGF controls epithelial-mesenchymal transitions during gastrulation by regulating cell division and apicobasal polarity

ABSTRACT To support tissue and organ development, cells transition between epithelial and mesenchymal states. Here, we have investigated how mesoderm cells change state in Drosophila embryos and whether fibroblast growth factor (FGF) signaling plays a role. During gastrulation, presumptive mesoderm cells invaginate, undergo an epithelial-to-mesenchymal state transition (EMT) and migrate upon the ectoderm. Our data show that EMT is a prolonged process in which adherens junctions progressively decrease in number throughout the migration of mesoderm cells. FGF influences adherens junction number and promotes mesoderm cell division, which we propose decreases cell-cell attachments to support slow EMT while retaining collective cell movement. We also found that, at the completion of migration, cells form a monolayer and undergo a reverse mesenchymal-to-epithelial transition (MET). FGF activity leads to accumulation of β-integrin Myospheroid basally and cell polarity factor Bazooka apically within mesoderm cells, thereby reestablishing apicobasal cell polarity in an epithelialized state in which cells express both E-Cadherin and N-Cadherin. In summary, FGF plays a dynamic role in supporting mesoderm cell development to ensure collective mesoderm cell movements, as well as proper differentiation of mesoderm cell types. Summary: FGF regulates epithelial-mesenchymal transition in mesoderm to support collective movement at gastrulation and also the reverse, mesenchymal-to-epithelial transition, during which cells acquire apicobasal polarity to support their differentiation into diverse muscle types.