CONTROL OF DISTAL ANTENNAL IDENTITY AND TARSAL DEVELOPMENT IN DROSOPHILA BY SPINELESS-ARISTAPEDIA, A HOMOLOG OF THE MAMMALIAN DIOXIN RECEPTOR

We report the molecular characterization of the spineless (ss) gene of Drosophila, and present evidence that it plays a central role in defi ning the distal regions of both the antenna and leg. ss encodes the cl osest known homolog of the mammalian dioxin receptor, a transcription factor of the bHLH-PAS family. Loss-of-function alleles of ss cause th ree major phenotypes: transformation of distal antenna to leg, deletio n of distal leg (tarsal) structures, and reduction in size of most bri stles. Consistent with these phenotypes, ss is expressed in the distal portion of the antennal imaginal disc, the tarsal region of each leg disc, and in bristle precursor cells. Ectopic expression of ss causes transformation of the maxillary palp and distal leg to distal antenna, and induces formation of an ectopic antenna in the rostral membrane. These effects indicate that ss plays a primary role in specifying dist al antennal identity. In the tarsus, ss is expressed only early, and i s required for later expression of the tarsal gene bric a brac (bab). Ectopic expression causes the deletion of medial leg structures, sugge sting that ss plays an instructive role in the establishment of the ta rsal primordium. In both the antenna and leg, ss expression is shown t o depend on Distal-less (Dll), a master regulator of ventral appendage formation. The antennal transformation and tarsal deletions caused by ss loss-of-function mutations are probably atavistic, suggesting that ss played a central role in the evolution of distal structures in art hropod limbs.