Df(1)btd-Sp1 homozygotes are lethal during the embryonic stage. Full leg Df(1)btd-Sp1 homozygous clones result in complete leg loss or small stumps with residual leg tissue.

Df(1)btd-Sp1 homozygous clones that span leg segments result in segment fusion, usually associated with segment shortening, whereas clones occurring near the distal end of leg segments lead to small outgrowths, as compared to controls.

Df(1)btd-Sp1 mutant clones, initiated during the second instar or before, survive poorly in most of the leg disc, except for the most proximal domain which gives rise to the body wall. Clones are readily recovered in wing, haltere and eye imaginal discs. Cell death (assayed using Caspase 3 staining) is seen in the few surviving ventral discs, but is not detected in the dorsal imaginal discs.

Legs composed entirely of Df(1)btd-Sp1 clone cells (generated in a minute background in the second instar larval stage) are reduced in size compared to controls. Growth defects are observed throughout the entire leg, from the coxa to the tip of the tarsus. However, bracted bristles are present. When clones are generated in the antenna, the a1 and a2 segments are severely reduced, whereas the a3 and arista segments are unaffected. Df(1)btd-Sp1 mutant wings and haltere clones do not exhibit any phenotypes.

Flies containing Df(1)btd-Sp1 mutant clones (generated in a minute background during embryogenesis using Scer\FLP1^UAS.cUa under the control of Scer\GAL4^Dll-em212) have severely aberrant legs. In 90% of adults, the legs are completely absent or consist of only a small patch of residual leg tissue. Leg discs clones comprised entirely of mutant tissue are reduced in size. Ventral to dorsal transformations are also seen in approximately 10% of these flies. Int he affected flies, one or two of the legs are transformed into elements of the wing, haltere and notum. This wing tissue is observed in T1 and T2, and to a lesser extent in T3.