The Role of Sexuality in Dosage

PROBLEMS of genetic regulation have received increasing attention in recent years and controlling mechanisms are being elucidated with great rapidity. One such problem, that of dosage compensation, was originally defined in Drosophila, and, for nearly thirty years, its mechanism of action has remained open to question. The term “dosage compensation” indicates that, for sex-linked genes which differ in dose between males and females, there is a regulatory mechanism operating such that the resultant phenotypes of these X-linked genes are equivalent in the two sexes. Two main theories have been proposed to account for dosage compensation in Drosophila. The first, suggested by STERN (1929, as quoted in STERN, 1960) but later elaborated and tested by MULLER (1932, 1950) postulates that the compensatory action is brought about by modifier genes which have evolved to equalize the phenotypes of the sexes so as to eliminate any differential selection which might endanger the continued perpetuation of the species. The second theory, espoused by GOLDSCHMIDT (1954), proposed that males and females were inherently different physiological systems and that dosage compensation was brought about by this difference which was established by the sex determining genes. GOLDSCHMIDT contended that one developmental mechanism based on differing physiologies could explain not only dosage compensation but also cases of autosomal dimorphism, whereby males and females exhibit different phenotypes for genes present in the same dose in the two sexes. Although GOLDSCHMIDT was unable to unequivocably substantiate his hypothesis, recent evidence ( KOMMA, 1966) has suggested that differing sex physiologies may play a role in the regulation of the sex-linked enzyme, glucose-6-phosphate dehydrogenase (G-6-PD) . In order to examine more fully the possibility that sex physiology plays a role in dosage compensation and attempt to elucidate a unifying mechanism to explain not only X chromosome regulation in Drosophila but also cases of autosomal dimorphism, in which the male always seems to appear more wild-type than the female ( LINDSLEY and GRELL, 1968), the following experimental scheme was employed. The third chromosome sex transformation gene, doublesex (dsz: HILDRETH and LUCCHESI 1963; HILDRETH 1965), which converts chromosomal