Male sexual signaling is defective in mutants of the apterous gene of Drosophila melanogaster.

Abstract

The apterous (ap) gene of Drosophila melanogaster exhibits extreme pleiotrophy: its functioning is essential for life, normal wing structure, juvenile hormone production, female fertility, and normal development of female sexual receptivity. Four mutant ap alleles (ap4, ap56f, apc, and apblt) were characterized for three additional phenotypes: male mating success, courtship behavior, and immature male sex appeal (the ability of males to stimulate homosexual courtship). Mating success with mature wild-type virgin females is reduced in males mutant for the ap gene, the extreme case being ap4/ap4 males, which are behaviorally sterile. In ap mutants, nonwing courtship elements are qualitatively like those of ap+/ap+ males. However, the mean rate of nonwing courtship directed toward virgin wild-type females (i.e., the mean temporal frequency of these displays) is reduced in males homozygous for ap4, ap56f, or apc alleles. In contrast, the apblt allele makes for wild-type rates of nonwing courtship. Immature male sex appeal persists for at least 3 days in males homozygous for apc and, to a lesser extent, in ap56f or ap4 homozygotes; apblt/apblt and wild-type males lose immature male sex appeal after 1 day. All three male phenotypes map to the ap locus, which is therefore essential for the development of normal levels of male courtship and male mating success and for the timely loss of immature male sex appeal. For each phenotype, ap+ is dominant to ap alleles making for behavioral abnormalities, with a single exception (for rate of nonwing courtship, ap+/apc was low). For mating success and frequency of nonwing courtship, each allele pair exhibits at least partial complementation, except for ap4 and ap56f, which fail to complement. For immature male sex appeal, apc, ap4, and ap56f fall into the same complementation group. Juvenile hormone production is not correlated with effects on male reproductive behavior.