The rapid and orderly folding of epithelial tissue during developmental processes such as gastrulation requires the precise coordination of changes in cell shape. Here， we report that the perforin-like protein Torso-like (Tsl)， the key extracellular determinant for embryonic terminal patterning， also functions to control epithelial morphogenesis. We find that null mutants display a ventral cuticular hole phenotype that is independent of the loss of terminal structures， and arises as a consequence of mesoderm invagination defects. We show that the holes are caused by uncoordinated constriction of ventral cell apices， resulting in the formation of an incomplete ventral furrow. Consistent with these da... More
The rapid and orderly folding of epithelial tissue during developmental processes such as gastrulation requires the precise coordination of changes in cell shape. Here， we report that the perforin-like protein Torso-like (Tsl)， the key extracellular determinant for embryonic terminal patterning， also functions to control epithelial morphogenesis. We find that null mutants display a ventral cuticular hole phenotype that is independent of the loss of terminal structures， and arises as a consequence of mesoderm invagination defects. We show that the holes are caused by uncoordinated constriction of ventral cell apices， resulting in the formation of an incomplete ventral furrow. Consistent with these data， we find that loss of is sensitive to gene dosage of ， a critical mediator of Rho1-dependent ventral cell shape changes during furrow formation， suggesting that Tsl may act in this pathway. In addition， loss of strongly suppressed the effects of ectopic expression of Folded Gastrulation (Fog)， a secreted protein that promotes apical constriction. Taken together， our data suggest that Tsl controls Rho1-mediated apical constriction via Fog. Therefore， we propose that Tsl regulates extracellular Fog activity to synchronize cell shape changes and coordinate ventral morphogenesis in Identifying the Tsl-mediated event that is common to both terminal patterning and morphogenesis will be valuable for our understanding of the extracellular control of developmental signaling by perforin-like proteins.
