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Fig. 2. Genetic interactions between LIM-HOM proteins and Ap function. (A) Leg of an apGal4/ap^UGO35 fly. The fourth tarsal segment is almost completely lost and is fused to the fifth (arrowhead), whereas the other leg segments are normal. (B) Rescue of the apGal4/Df(2)nap1 leg mutant phenotype by overexpression of an ap transgene. The ap mutant phenotype is completely rescued by one copy of the UAS-ap construct (compare with A and Fig. 1A). (C) Rescue of an apGal4/Df(2)nap1 leg mutant phenotype by overexpression of the chimaera protein Chip-Ap, consisting of Chip lacking the LIM interaction domain (LID) linked to Ap lacking the LIM domains. (D) Leg of an apGal4/Df(2)nap1;UAS-Lim3:ap-HD fly. Ectopic expression of a chimaera protein, which consists of the LIM domains of Lim3 and the Ap homeodomain, rescues the ap mutant phenotype. (E) apGal4;UAS-isl leg lacking the fourth tarsal segment. (F) Leg of an apGal4/UAS-ap;UAS-isl fly. Overexpression of Ap does not overcome the dominant-negative effect produced by ectopic Islet expression (compare with E). (G-G'') Leg imaginal disc of an apGal/UASGFP;UAS-islet larva. Ectopic expression of Islet does not affect either Ap or Bar expression. (G) Bar protein distribution (blue). (G') apGal4 expression (red). (G'') Merged image.

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