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Introduction
In mammals, sex is determined by the presence or absence of the Y chromosome. The first event in sexual differentiation is the differentiation of the bipotential gonad into testes or ovaries. All subsequent sexual differentiation is under hormonal control of the testes or ovaries. The genetic entity on the Y chromosome required for testis development has long been known as the testis-determining factor (TDF).
For the scientist, the joy of sex determination stems from the supposition that mutations in sex determination are not early embryonic lethals but sex reversing. Sex-reversed patients facilitate the mapping and identification of the genes involved in sex determination. The cloning of the genes will allow us to extend our understanding of the biochemistry and cell biology of sex determination.
Approximately 80% of XX males are sex reversed due to X-Y translocations in which TDF is transferred to the X chromosome. As for the remaining
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Soon after the sex steroid hormones were first identified, isolated and synthesized, they were found to have potent effects on sex determination and sexual differentiation in various fish, amphibians, reptiles and, to a lesser extent, birds (reviewed in Burns 1961). However, there was no evidence that these chemicals could influence gonadal differentiation in mammals, although they were recognized to mediate differentiation of accessory and secondary sex characteristics. Indeed, conventional wisdom today holds that steroid hormones play no role in sex determination in mammals, and it is only following gonadal differentiation that steroid hormones produced by the ovaries or testes sculpt the characters that distinguish males from females. Thus, with the exception of limited research in aquaculture and poultry science, the study of the role of sex hormones in vertebrate sex determination essentially ceased by midcentury, with the result that current texts focus on the molecular genetics of sex determination in
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ABSTRACT
Changes in plasma concentrations of sex steroids were examined in male and female zebra finch chicks during the sensitive period for differentiation of sexually dimorphic brain nuclei associated with the control of song. Using a chromatographic separation procedure and radioimmunoassay, androstenedione, testosterone and 5α-dihydrotestosterone were detected in plasma at relatively high concentrations immediately after hatching. There were no sex differences in concentrations of these androgens. An oestrogen, oestradiol-17β, which is known to differentiate the song-control system, is raised specifically in the circulating plasma of male zebra finch chicks, and not in females. The surge in oestradiol, which occurs during the first week after hatching, coincides with the period when capacity for differentiation of the song system is maximal. Exposure of the male brain to oestradiol-17β could trigger neuronal differentiation.
J. Endocr. (1984) 103, 363–369
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ABSTRACT
Rat liver exhibits a reversed sexual dimorphism of its two endogenous soluble carbonic anhydrase (CA) isozymes, CA II and CA III. Normal males have hepatic CA III concentrations ten–twenty times those in the female, while female liver contains two–three times more CA II than the male. Hypophysectomy abolishes this sexual differentiation, having no effect on male liver but producing isozyme concentrations in the female liver similar to those in the male. Infusion of a continuous level of GH into male rats induces a female-like isozyme pattern for both CA II and CA III.
J. Endocr. (1986) 110, 123–126
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The primary function of MIS in mammals is to initiate regression of Mullerian structures in males as part of normal sexual development. As we learn more about its other roles, particularly its influence on the growth and differentiation of cell types within the gonad, a more thorough understanding of the receptors that MIS stimulates and the downstream signaling cascade with which it interacts will help in the development of diagnostic and therapeutic uses of MIS.
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Sexual differentiation and early embryonic/fetal gonad development is a tightly regulated process controlled by numerous endocrine and molecular signals. These signals ensure appropriate structural organization and subsequent development of gonads and accessory organs. Substantial differences exist in adult reproductive characteristics in Meishan (MS) and White Composite (WC) pig breeds. This study compared the timing of embryonic sexual differentiation in MS and WC pigs. Embryos/fetuses were evaluated on 26, 28, 30, 35, 40 and 50 days postcoitum (dpc). Gonadal differentiation was based on morphological criteria and on localization of GATA4, Mullerian-inhibiting substance (MIS) and 17alpha-hydroxylase/17,20-lyase cytochrome P450 (P450(c17)). The timing of testicular cord formation and functional differentiation of Sertoli and Leydig cells were similar between breeds. Levels of GATA4, MIS and P450(c17) proteins increased with advancing gestation, with greater levels of MIS and P450(c17) in testes of MS compared with WC embryos. Organization of ovarian medullary cords and formation of egg nests was evident at similar ages in both breeds; however, a greater number of MS compared with WC embryos exhibited signs of ovarian differentiation at 30 dpc. In summary, despite breed differences in MIS and P450(c17) levels in the testis, which may be related to Sertoli and Leydig cell function, the timing of testicular differentiation did not differ between breeds and is unlikely to impact reproductive performance in adult boars. In contrast, female MS embryos exhibited advanced ovarian differentiation compared with WC embryos which may be related to the earlier reproductive maturity observed in this breed.
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Castration or treatment with an anti-androgen of male rats immediately after birth favours a female differentiation of the hypothalamic mating centre(s). Treatment of such animals with oestrogen when grown up causes female sexual behaviour (Feder & Whalen, 1965; Grady, Phoenix & Young, 1965; Neumann & Elger, 1966).
In genuine homosexuality of human males there is, however, a normal or at least nearly normal androgen level after puberty. Therefore, a satisfactory hormonal explanation of genuine male homosexuality is only possible if androgens were also able to induce predominantly receptive female activity in a geno- and phenotypically male organism. This 'homosexual model' was produced in animal experiments, in which it was shown that male rats castrated neonatally and treated with androgen when adult displayed predominantly female sexual behaviour (Dörner, 1967).
In the present experiments this 'homosexual model' was re-investigated. Furthermore, the possibility of preventing androgen-induced feminine sexual behaviour by androgen administration during
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Male rats were treated daily with oil or 100 μg of the antioestrogen, ethamoxytriphetol (MER-25), for the first 10 days of life and, when adult, lesions were made in the suprachiasmatic nuclei (SCN) of the hypothalamus or control lesions were made above the SCN and the rats were tested for sexual behaviour. Treatment with MER-25 enhanced the daily rhythmicity in both mounting and lordosis behaviour and SCN lesions disrupted these behavioural rhythms and the rhythm in the mounting behaviour of oil-treated rats. Rats treated with MER-25 and with SCN lesions showed high levels of mounting and lordosis behaviour throughout the light: darkness cycle. These results support the hypothesis that sexual differentiation by perinatal androgen stimulation uncouples the central rhythm generator from the neural substrates of sexual behaviour in rats.
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Different degrees of permanent gonadal insufficiency and deviations of sexual behaviour have been produced in male and female rats treated with high doses of androgen or oestrogen during the perinatal phase of hypothalamic organization (Harris, 1964; Dörner, 1968, 1969a, b). In this study, the endogenous sex hormone level was increased by gonadotrophin administration in this critical period of hypothalamic differentiation and its effect on gonadal function and sexual activity in adult rats of both sexes was investigated.
Twenty-nine male and 20 female Sprague-Dawley rats were injected s.c. daily for the first 14 days of life with 10 i.u. human chorionic gonadotrophin (HCG) in 0·1 ml. water. Twenty-six males and 18 females, which received the solvent only, served as controls. On day 15, eight animals of each group were killed. Vaginal smears from the remaining females were examined daily during the 3rd month of life and sexual behaviour and fertility
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In many species of oviparous reptiles, the first steps of gonadal sex differentiation depend on the incubation temperature of the eggs. Feminization of gonads by exogenous oestrogens at a male-producing temperature and masculinization of gonads by antioestrogens and aromatase inhibitors at a female-producing temperature have irrefutably demonstrated the involvement of oestrogens in ovarian differentiation. Nevertheless, several studies performed on the entire gonad/adrenal/mesonephros complex failed to find differences between male- and female-producing temperatures in oestrogen content, aromatase activity and aromatase gene expression during the thermosensitive period for sex determination. Thus, the key role of aromatase and oestrogens in the first steps of ovarian differentiation has been questioned, and extragonadal organs or tissues, such as adrenal, mesonephros, brain or yolk, were considered as possible targets of temperature and sources of the oestrogens acting on gonadal sex differentiation.In disagreement with this view, experiments and assays carried out on the gonads alone, i.e. separated from the adrenal/mesonephros, provide evidence that the gonads themselves respond to temperature shifts by modifying their sexual differentiation and are the site of aromatase activity and oestrogen synthesis during the thermosensitive period. Oestrogens act locally on both the cortical and the medullary part of the gonad to direct ovarian differentiation. We have concluded that there is no objective reason to search for the implication of other organs in the phenomenon of temperature-dependent sex determination in reptiles. From the comparison with data obtained in other vertebrates, we propose two main directions for future research: to examine how transcription of the aromatase gene is regulated and to identify molecular and cellular targets of oestrogens in gonads during sex differentiation, in species with strict genotypic sex determination and species with temperature-dependent sex determination.
