Signals beneath the ectoderm: Mesodermal FGF signaling keeps the dorsally closing epithelium in shape
Morphogenesis requires coordinated biochemical signaling, actomyosin contractility and dynamic adhesion within and between tissues. During Drosophila development, ectodermal fibroblast growth factor (FGF) ligands regulate mesoderm morphogenesis through the FGF receptor (FGFR) Heartless. We find that the mesoderm reciprocally influences ectodermal morphogenesis. We show that loss of the FGF ligands Pyramus or Thisbe, Heartless, or its adaptor Stumps transforms normally straight dorsal seams and the formed dorsal epidermis into highly distorted, dynamically changing zigzags during dorsal closure. In these mutants, mesoderm is specified but defective. Mesodermal expression of Heartless restores epithelial stability in heartless mutants, whereas ectodermal expression does not. Genetic ablation of mesoderm produces more extensive seam distortions that persist beyond the end of closure, thereby displacing the dorsal midline. Despite these striking deformations, closure continues to completion. Together, our findings reveal a non-cell-autonomous requirement for mesodermal FGFR signaling in stabilizing the closing ectoderm and its newly formed seams. They identify a reciprocal influence of mesoderm on the ectoderm that patterns it and show that stable tissue geometry can be uncoupled from successful completion of a morphogenetic movement.