Expression of AP-2^Scer\UAS.cMa under the control of Scer\GAL4^AP-2.E6 partially rescues the AP-2²/AP-2¹⁵ leg phenotypes. In some cases, an almost complete rescue of the outgrowth defect in the proximal and intermediate leg segments (coxa, trochanter, femur and tibia) is observed. In the distal leg, Scer\GAL4^AP-2.E6-driven AP-2^Scer\UAS.cMa significantly rescues the outgrowth defect of the tarsus, but fails to restore tarsal joints.

AP-2²/AP-2¹⁵ mutant males display a reduced accessory gland size, vas deferens are narrower at their distal ends, and the anterior ejaculatory ducts less bulbous.

Heterozygotes with AP-2^stummelbein show a similar mutant short-leg/no joint phenotype as do AP-2^stummelbein homozygotes. Early stages of axial patterning of the leg disc appear normal.

Pharate pupae and the few eclosing adults show a short leg phenotype. Leg length = 30% wild type. Tarsal joints are lacking. Legs are non-functional. The proximodistal order of segments is not grossly affected as landmarks for the coxa, femur, tibia, and first and last (5th) tarsal segments (sex comb and claws, respectively) are present in the correct order. Rows of misoriented sensory bristles indicate that proximodistal polarity is locally perturbed. The stunted legs show no nervous activity except for a faint twitching of the claws and of cuticle over the femur-tibia junction. The proboscis is reduced in length and width. Null mutants show a substantial reduction in length and width of the labellum and number of pseudo tracheal rows. The prestomal cavity is present and newly eclosed adults can drink. Clypeus, maxillary palps and antennae are apparently normal but there is increased spacing between antennae. Mutants lack gross defects in the embryonic brain.