Abstract
Folded gastrulation (Fog), a secreted ligand for a G protein-coupled receptor (GPCR), is a key regulator of cell shape changes during epithelial morphogenesis. During Drosophila embryogenesis, fog is expressed in multiple invaginating tissues, including the mesoderm, salivary gland, and trachea. In the mesoderm and salivary gland, Fog signaling coordinates apical constriction through Rho kinase (Rok)-mediated myosin activation; however, its role in tracheal morphogenesis remains unresolved. Here, we investigate Fog function in the developing trachea, using both loss- and gain-of-function analyses. In contrast to its role in other epithelial tissues, Fog does not regulate Rok or myosin in the trachea, and tracheal invagination proceeds largely normally following either loss or overexpression of fog. Consistent with these findings, Fog overexpression fails to induce medioapical accumulation of Rok or myosin in tracheal cells and does not promote apical recruitment of its receptor, the Smog GPCR, in tracheal epithelia, unlike in the salivary gland or ectoderm. Although fog mutant embryos exhibit late-stage tracheal abnormalities, including convoluted branches and occasional gaps in the dorsal trunk, these correlate with broader morphological defects rather than a tracheal-specific requirement for Fog. Together, our results demonstrate that tracheal invagination proceeds independently of Fog signaling, underscoring the tissue-specific nature of Fog function during embryogenesis.
