Open AccessFGF controls epithelial-mesenchymal transitions during gastrulation by regulating cell division and apicobasal polarity
Author(s) -
Jui-Hung Sun,
Angelike Stathopoulos
Publication year - 2018
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.161927
Subject(s) - mesoderm , adherens junction , microbiology and biotechnology , gastrulation , biology , fibroblast growth factor , cell polarity , ectoderm , epithelial–mesenchymal transition , fgf and mesoderm formation , cadherin , cell , embryogenesis , embryo , embryonic stem cell , genetics , transition (genetics) , receptor , gene
To support tissue and organ development, cells transition between epithelial and mesenchymal states. Here we 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 mesoderm cells’ migration. 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 beta-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.