The apterous (ap) gene in Drosophila melanogaster encodes a homeodomain transcription factor. It is required for the development of the wings and of a subset of embryonic muscles. The gene has been implicated in the juvenile hormone (JH) system because mutations in ap lead to JH deficiency, and are associated with defective histolysis of the larval fat body, arrested vitellogenesis, sterility, and aberrant sexual behavior, all of which are dependent on JH. We describe here the use of hemizygotes and germ-line clones, of X-ray- and hybrid dysgenesis-induced lethal ap alleles to determine the primary role of the gene during development. We find that ap lethality is polyphasic, but occurs primarily at the larval and pupal stages. The lethal phenotype is not associated with any overt morphological abnormality, suggesting that death occurs from a systemic malfunction. Strong interallelic complementation for the wing phenotype was found between some ap mutations induced by X-rays or by hybrid-dysgenesis. By Northern blot analysis, we demonstrate an increase in ap expression in pupae and adults as compared to embryos and larvae, suggesting that it is developmentally regulated. Finally, primer extension is used to determine the transcription start site of the gene.