Global tissue rotation was proposed as a morphogenetic mechanism controlling tissue elongation. In Drosophila ovaries, global tissue rotation of egg chambers coincides with egg chamber elongation. Egg chamber rotation was put forward to result in circumferential alignment of actin filaments and extracellular fibers. These fibers serve as molecular corsets to restrain growth of egg chambers perpendicular to the anteroposterior axis, thereby leading to the preferential egg chamber elongation along this axis. The atypical cadherin Fat2 is required for egg chamber elongation, rotation, and the circumferential alignment of actin filaments and extracellular fibers. The localization of Fat2 protein at the basal side of follicle cells is planar polarized. Fat2 protein is enriched on cell junctions oriented parallel to the long axis of the egg chamber. The functional relationship between Fat2 planar polarized localization, egg chamber rotation and egg chamber elongation, however, remained unclear.
Here we have generated a truncated form of Fat2 that lacks its entire intracellular region. fat2 mutant egg chambers expressing this truncated protein display normal actin and extracellular fiber alignment and properly elongate. However, the localization of the truncated Fat2 protein is not planar polarized and these egg chambers fail to rotate. Our data for the first time uncouple Fat2 planar polarization and global tissue rotation from egg chamber elongation. Thus global tissue rotation, even though coinciding with tissue elongation, is not a necessary prerequisite for elongation.