Large mutant follicle cell clones induce the formation of compound egg chambers that contain several cysts. The oocytes preferentially contact mutant follicle cells in these cysts.

Homozygous follicle clone cells show no defect in F-actin organisation at stage 6. However, at stage 12, defects in basal actin filament organisation are seen in these cells.

rhea^unspecified mutant embryos muscle cells become detached from the epidermis and from each other and muscle-tendon cell junctions that remain are abnormal. In the tendon cells microtubules extend from apical tonofibrils toward the basal membrane, but mature basal attachment sites fail to form. Structural features of normal attachment sites, such as extensive folding of basal membranes and linkage of microtubules to the inner surface of basal membranes are generally not present. In addition, the microtubules are abnormally oriented, in some cases running parallel, rather than perpendicular, to the exoskeleton. On the muscle cell side of the junction, the actin cytoskeleton is disorganised. There is also a reduction in the amount of electron-dense material on the cytoplasmic face of hemiadherens junctions at muscle attachment sites.