Search

The effect of diethylstilboestrol on gonad development in quail embryos has been quantitatively analysed. Quail embryos at 4 days of incubation were treated with diethylstilboestrol (DES), using the egg dipping method. At 10 days of incubation, embryos were removed and killed by decapitation. Tissues were prepared for chromosome analysis, and the parts of the abdomen containing the gonads were prepared for serial sectioning and quantitative assessment. Left gonads of DES-treated male embryos resembled ovaries histologically, while their right gonads were markedly reduced in size. Right gonads of DES-treated female embryos were also further reduced by treatment with DES. There was no statistically significant effect by DES treatment on the size of left gonads, although the ratio of left compared with right gonadal volumes was highly significant. Since, in birds, the left embryonic gonad has ambisexual potential, while the potential of the right gonad is exclusively masculine, these results exemplify the adverse effect exerted by oestrogen on male sexual development in vertebrates.

Growth and histological differentiation were studied in 8 litters of embryos and 4 litters of neonate grey short-tailed opossums, Monodelphis domestica. The embryonic litters included 2 that had passed their expected birth date, and whose weights exceeded the usual birthweights; we refer to these litters as 'postmature'. There was an abrupt increase in the growth rate of XY gonads after birth, but this was not seen in XX gonads. Although there was evidence of testicular differentiation in XY gonads on the day before the expected birth, testicular differentiation was found to be blocked in postmature litters. The growth of XX gonads in postmature embryos was not affected. In view of evidence that exogenous oestrogens feminise the gonads of genetic males in some species of marsupials including Monodelphis domestica, the question arises whether oestrogen is responsible for the failure of testes to continue their development in utero. We suggest that the ability of functional testes to develop in the presence of oestrogen may be a fundamental requirement distinguishing eutherian mammals from other vertebrates, including marsupials.

A quantitative and histological study of the gonads of newborn grey short-tailed opossums, Monodelphis domestica, is described. The pups were karyotyped, and comparisons were made within litters segregating for XX and XY sex chromosomes. A total of four litters including 25 pups were available. On the day of birth, developing testes were significantly larger than the ovaries of litter mates, and testes could be histologically distinguished by the formation of sex cords and a tunica albuginea. The data suggest that in this marsupial species gonadal differentiation may be initiated in utero.

The evolutionary conservation of H-Y antigen and its expression in the heterogametic sex regardless of whether this is male or female must mean that the antigen is associated with a common denominator underlying the development of mammalian testes and avian ovaries. It is suggested that one such common denominator is an enhanced growth rate of the dominant heterogametic gonad at a critical stage of its development.

In human hermaphrodites, testes are preferentially situated on the right and ovaries on the left side. This asymmetry can be related to the results of measurements on the growth of fetal gonads. Testes exceed ovaries in weight, protein and DNA contents in fetuses of the same crown-rump length, and in both sexes, right gonads exceed left gonads in the same criteria. These findings, support the hypothesis that in mammals, a basic growth rate will convert the bipotential gonadal rudiment into an ovary while an increased growth rate is required for testicular development. Relative growth rates of chick embryo gonads are largely, although not entirely, the opposite of those in mammals: during the major period of gonadal differentiation, the ovary exceeds the testes in growth. The expression of H-Y antigen in birds and mammals seems to correspond to the presence of the faster growing gonad. These data do not support the hypothesis that H-Y antigen is the primary determiner of sex but a secondary involvement is likely.

Oocyte counts carried out in 3- to 5-day-old tertiary trisomic Ts(512)31H mice revealed a mean reduction of 71% in the number of oocytes as compared with that of normal littermates. The pool of small oocytes was reduced by 75%, and the number of growing oocytes by 8%. The sperm count of the trisomic males was less than 1% of normal, with most spermatozoa being abnormal (Beechey et al., 1980). These results indicate that the presence of the extra 512 chromosome, which causes male sterility, also has a marked effect on oogenesis. Possible reasons for the difference in severity of the gametogenic impairment in males and females are discussed.

Whole-mount preparations of silver-stained spermatocytes and oocytes from Ts(512)31H mice were examined in the electron microscope. The 5(12) chromosome was associated with the XY bivalent in the large majority of spermatocytes, whereas in about one-half of the oocytes, the 5(12) was associated with either unpaired chromosomes or heterochromatic parts of chromosomes or showed self-synapsis. There was a tendency for 5(12) chromosomes to be more fully heterochromatic in oocytes than in spermatocytes. A large proportion of oocytes (50%) and a much smaller proportion of spermatocytes exhibited various errors of chromosome pairing, but these proportions were only marginally greater than in control gametocytes from mice with normal karyotypes. It is concluded that the observed errors of pairing bear no simple relation to the almost complete breakdown of spermatogenesis and the marked impairment of oogenesis that occur in tertiary trisomic Ts(5(12))31H mice.

It is now evident that variations in chromosome constitution may have a profound effect on physical and mental development, both normal and pathological. Mongolism is the best known example of a severe congenital abnormality caused by the presence of an additional chromosome; while a difference in the sex chromosome constitution-XY in the male and XX in the female-produces the most far-reaching normal variation in human beings and other animal species. In spite of the spectacular progress in our knowledge of human chromosomes during the past 15 years, there is as yet no working hypothesis relating cause and effect; in other words, we need an answer to the question: 'By what mechanism do different chromosome constitutions result in different end products of development?'