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PubMed2005

Conserved expression of a novel gene during gonadal development.

We isolated the novel gene Gonad Expressed Transcript (GET) from a chicken embryonic gonad library enriched for differentially expressed male transcripts. Chicken GET encodes a predicted protein containing a Pfam-B 30624 domain with homology to a putative orthologue in mammals. Chicken GET expression was confined to the developing urogenital system. It was first detected in the glomerulus of the mesonephros of both sexes from embryonic day (E) 2.5. At E4.5, expression switches to the gonad of both sexes and then localizes to the gonadal cortex. We isolated the putative mouse orthologue and examined expression in the mouse embryo. Gonadal expression was conserved. Ovarian expression localized to the cortex as in the chicks. However, in contrast to the chicken, testis expression localized to the cords. In the adult, GET is expressed in the ovary but not the testis of both the chicken and the mouse. Expression of GET in the müllerian duct, wolffian duct, metanephric kidney, and external genitalia, suggests that GET may play a wider role in the development of the urogenital system.

Amino Acid Sequence↗
PubMed1998

Differential expression of genes for aromatase and estrogen receptor during the gonadal development in chicken embryos.

In birds, differentiation of embryonic gonads is not as strictly determined by the genetic sex as it is in mammals, and can be influenced by early manipulation with a sex steroid hormone. Thus administration of an aromatase inhibitor induces testis development in the genetic female, and administration of estrogen induces a left ovotestis in the genetic male embryo. Another feature of avian gonadogenesis is that only the left ovary develops in most species. Molecular mechanisms underlying these features at the level of gene expression have not been elucidated. In this paper, we present evidence that a gene for aromatase cytochrome P-450, an enzyme required for the last step in the synthesis of estradiol-17beta, is expressed in medullae of the left and right gonads of a female chicken embryo, but not in those of a male chicken embryo, and that an estrogen receptor gene is expressed only in epithelium (and cortex later, in the female) of the left, not the right, gonad of both sexes, but the expression in the male left gonad is temporary and restricted to an early stage of development. Differential expression of these two genes serves well to explain the above features of gonadal development in birds. Furthermore, in ovo administration of estradiol-17beta from the 5th to the 14th day of incubation does not cause expression of the estrogen receptor gene in the right gonad of chicken embryos of either sex, suggesting that the absence of expression of the estrogen receptor gene in the right gonad is not the result of down-regulation, but may be regarded as an important cause of the unilateral ovarian development.

Animals↗
PubMed2001

An overview of factors influencing sex determination and gonadal development in birds.

The morphological development of the embryonic gonads is very similar in birds and mammals, and recent evidence suggests that the genes involved in this process are conserved between these classes of vertebrates. The genetic mechanism by which sex is determined in birds remains to be elucidated, although recent studies have reinforced the contention that steroids may play an important role in the structural development of the testes and ovaries in birds. So far, few genes have been assigned to the avian sex chromosomes, but it is known that the Z and W chromosomes do not share significant homology with the mammalian X and Y chromosomes. The commercial importance of poultry breeding has motivated considerable investment in developing physical and genetic maps of the chicken genome. These efforts, in combination with modern molecular approaches to analyzing gene expression, should help to elucidate the sex-determining mechanism in birds in the near future.

Animals↗
PubMed2001

Effect of exogenous growth hormone on somatic growth, gonadal development, and hepatic CYP2C11 and CYP2C12 expression in prepubertal intact male rats.

The influence of exogenous growth hormone (GH) on pubertal maturation, as assessed by growth, age of preputial separation, testicular development, and hepatic expression of sexually dimorphic cytochrome P450 (CYP) enzymes, was investigated. Treatment of 22-day old prepubertal intact male rats with twice daily subcutaneous (s.c.) injections of rat recombinant GH (0.12 microg/g body weight) for 12 or 21 days did not affect body weight, skeletal growth, or testicular weight. By comparison, GH suppressed hepatic CYP2C1 enzyme activity, protein, and mRNA levels but induced CYP2C12 expression. GH suppressed CYP2C11 expression by approximately 60% in prepubertal rats as compared with 30% in adult rats, whereas it increased CYP2C12 levels to 80% of the normal female levels but had no effect in adult male rats. Twice daily intravenous injections of GH suppressed CYP2C11 only. Increasing the s.c. dose of GH 30-fold produced little or no additional change in CYP2C11 or CYP2C12 expression, whereas it modestly in creased body weight and skeletal growth and reduced testicular weight. Overall, the present study provides the first demonstration that prepubertal administration (22-33 days of age) of GH at a pharmacologically relevant dose (0.12 microg/g twice daily) suppressed hepatic expression of CYP2C11 in 34-day-old intact male rats, suggesting that in this age group the liver is intrinsically responsive to transcription factors involved in the regulation of GH-dependent, sex-specific CYP gene expression. A higher dose (3.6 microg/g) of GH administered during the prepubertal period was required to elicit a modest effect on somatic growth and gonadal development.

Animals↗
PubMed2006

Wnt4 action in gonadal development and sex determination.

Wnt4 is a growth factor involved in multiple developmental processes such as the formation of the kidney, adrenal, mammary gland, pituitary and the female reproductive system. During mammalian embryogenesis, Wnt4 is expressed in the gonads of both sexes before sex determination events take place and is subsequently down-regulated in the male gonad. Inactivation of the Wnt4 gene in mice has revealed that it is involved at several steps of female reproductive development. Wnt4 is implicated in Müllerian duct regression, the formation of sex-specific vasculature, the inhibition of steroidogenesis and in sex-specific cell migration events. A mouse model of sex-reversal has partially unravelled the molecular pathways in which Wnt4 operates during the development of the female reproductive system. However, the specific molecular mechanism of action of Wnt4 during gonadal development remains unknown. This and downstream signaling pathways involved in Wnt4 action during female gonad development are reviewed and models of Wnt4 action are proposed for Müllerian duct formation, sex-specific vasculature development, and sex determination events. Further identification of critical downstream effectors of the Wnt4 signaling pathway in mouse models and in patients with sex-reversal conditions could help in understanding sex-reversal pathologies in humans.

Animals↗
PubMed1999

Oncogenes and tumour suppressor genes in first trimester human fetal gonadal development.

Tumour suppressor genes and oncogenes that control proliferation and apoptosis are known to play an important role in embryogenesis, second trimester fetal oocyte loss, adult ovulation, and in adult male testicular degeneration. We have examined tumour suppressor genes, oncogenes and oestrogen receptors during first trimester human gonadal differentiation to investigate their role at this crucial phase in development. Immunohistochemistry was used to localize the gene products of Bcl-2, c-erB-2, c-myc, p53, nm23 and oestrogen receptor. As gonadal development occurred at 6-12 weeks gestation, a changing pattern of expression was observed that varied in different cell types. The oestrogen receptor was not present in oogonia, spermatogonia and supporting cells during the first trimester. This study highlights the importance of oncogenes and tumour suppressor genes in first trimester gonadal development.

Adult↗
PubMed2005

Mechanisms of Disease: normal and abnormal gonadal development and sex determination in mammals.

Sex differentiation in mammals occurs in three steps. The first is the establishment of chromosomal sex at fertilization, followed by the differentiation of the gonad into an ovary or testis, and finally the establishment of the phenotypic sex of the embryo and adult, which is regulated by the gonad. Disruption of any of these stages gives rise to sexual ambiguities that include 46,XY pure gonadal dysgenesis, 46,XX true hermaphroditism, and variable degrees of intersexuality. In this review, we focus on the development of the mammalian gonad from a bipotential primordium that differentiates into either an ovary or a testis. We describe the recent increase in our knowledge of the genetic defects that directly affect gonadal development, sex determination, and sex differentiation, with emphasis on the comparison of genetic studies in mice with studies of naturally occurring mutations in humans.

Animals↗
PubMed1999

Expression of anti-Müllerian hormone during normal and pathological gonadal development: association with differentiation of Sertoli and granulosa cells.

The ontogeny of expression of anti-Müllerian hormone (AMH) was examined by immunohistochemistry in 135 human gonadal tissue specimens of various developmental age, ranging from 6 weeks of fetal development to 38 yr of postnatal age. The series included specimens from normal testes and ovaries and from individuals either with pathological conditions affecting gonadal development or with idiopathic infertility manifested as azoospermia or severe oligozoospermia. AMH expression was found only in Sertoli and granulosa cells. A 6-week-old fetal testis at the indifferent gonad stage did not yet express AMH. The protein was first visible at 8.5 weeks of development, when sex cords have not yet been formed. Afterward, a majority of testicular specimens, including those from pathological conditions, strongly expressed AMH through fetal development and childhood until puberty. Markedly prolonged expression of AMH was observed in a 20-yr-old 46,XY female with androgen insensitivity syndrome, who retained prepubertal testicular morphology. In normal testes, the switch-off of AMH expression was usually associated with the appearance of primary spermatocytes, suggesting that their presence had an inhibitory effect on AMH. However, in adolescent boys lacking germ cells because of cancer treatment and in a majority of infertile adult men with idiopathic germ cell aplasia, AMH expression was also down-regulated despite the complete lack of spermatogenesis. The decrease in AMH expression thus reflects the terminal differentiation of Sertoli cells and is probably only partially dependent upon a regulatory factor associated with the onset of meiosis. In fetal ovaries, AMH was first detected at 36 weeks gestation in granulosa cells of preantral follicles. Thus, the onset of ovarian expression is at the end of fetal life and not in infancy as previously reported.

Adolescent↗
PubMed2005

Differential expression of neural and gonadal aromatase enzymatic activities in relation to gonadal development in Japanese eel, Anguilla japonica.

The objectives of the present study were to investigate the enzymatic characteristics of brain aromatase in Japanese eel, Anguilla japonica, as well as the correlations between aromatase activities in various tissues (brain regions, pituitary, and gonads) and ovarian development. Eel brain aromatase exhibited a K(m) of 75 nM and a V(max) of 1.14 fmol/min mg protein (91.5 fmol/h mg protein), indicating an enzymatic activity much lower than in other teleosts but similar to that in mammals. This supports the hypothesis of the occurrence of a single aromatase gene in eels (representative of an ancient group of teleosts, Elopomorphs), as in mammals, but unlike what is observed in more recent teleosts. Aromatase inhibitors could significantly suppress brain and pituitary aromatase activity. There was no significant sex difference in aromatase activity in the forebrain, midbrain, hindbrain, or pituitary, but there was in the gonads, where aromatase could be detected in the ovaries but not in the testes, in accordance with the role of this enzyme in ovarian differentiation. Comparison with another teleost, black porgy (Percomorph), under the same experimental conditions, further confirmed the low activity of aromatase in the eel. We investigated variations in brain, pituitary, and gonad aromatase activity in relation to ovarian development in control female eels (gonadosomatic index, GSI, 0.1-1.6%) as well as in eels treated with pituitary extract (experimental ovarian maturation; GSI up to 25%). Differential expression of neural and gonadal aromatase was observed in relation to the course of gonadal development. Pituitary aromatase activity increased with GSI at all stages. Brain (specially forebrain) aromatase activity significantly increased in early vitellogenic control eels (GSI>0.8%) and in treated eels. The low activity of eel aromatase may be related to the characteristic life cycle of the eel, in which there is a long delay of the onset of puberty before oceanic reproductive migration.

Androstenedione↗
PubMed2000

Gonadal development in mammals at the cellular and molecular levels.

In mammals, although sex is determined chromosomally, gonads in both sexes begin development as similar structures. Until recently it was widely held that female development constituted a "default" pathway of development, which would occur in the absence of a testis-determining gene. This master gene on the Y chromosome, SRY in the human and Sry in the mouse, is thought to act in a cell-autonomous fashion to determine that cells in the gonadal somatic population develop as pre-Sertoli cells. Triggering of somatic cell differentiation along the Sertoli cell pathway is therefore a key event; it was thought that further steps in gonadal differentiation would follow in a developmental cascade. In the absence of Sertoli cells, the lack of anti-Mullerian hormone would allow development of the female Mullerian duct and absence of Leydig cells would prevent maintenance of the Wolffian duct. Recent findings that female signals not only maintain the Mullerian duct and repress the Wolffian duct but also suppress the development of Leydig cells and maintain meiotic germ cells, together with the finding that an X-linked gene is required for ovarian development and must be silenced in the male, have shown that the female default pathway model is an oversimplification. Morphological steps in gonadal differentiation can be correlated with emerging evidence of molecular mechanisms; growth factors, cell adhesion, and signaling molecules interact together, often acting within short time windows via reciprocal control relationships.

Animals↗
PubMedDate not supplied

A cell-specific nuclear receptor plays essential roles in adrenal and gonadal development.

Recent analyses of the cytochrome P450 steroid hydroxylases have established a key role for an orphan nuclear receptor, designated steroidogenic factor 1 (SF-1), in their coordinate, cell-selective expression. SF-1 was proposed to regulate the steroid hydroxylases by interacting with shared promoter elements in their 5'-flanking regions. During mouse embryonic development, SF-1 was expressed from the earliest stages of organogenesis of the steroidogenic tissues, suggesting a key role in steroidogenic cell differentiation. Finally, disruption of the gene encoding SF-1 revealed its essential function in the development of the adrenal glands and gonads and in pituitary gonadotrope function. These studies suggest that SF-1 acts at multiple levels of the reproductive axis to maintain reproductive competence.

Adrenal Glands↗
PubMed1999

Gene interactions in gonadal development.

The acquisition of a sexually dimorphic phenotype is a critical event in mammalian development. Although the maturation of sexual function and reproduction occurs after birth, essentially all of the critical developmental steps take place during embryogenesis. Temporally, these steps can be divided into two different phases: sex determination, the initial event that determines whether the gonads will develop as testes or ovaries; and sexual differentiation, the subsequent events that ultimately produce either the male or the female sexual phenotype. A basic tenet of sexual development in mammals is that genetic sex--determined by the presence or absence of the Y chromosome--directs the embryonic gonads to differentiate into either testes or ovaries. Thereafter, hormones produced by the testes direct the developmental program leading to male sexual differentiation. In the absence of testicular hormones, the pathway of sexual differentiation is female. This chapter reviews the anatomic and cellular changes that constitute sexual differentiation and discusses SRY and other genes, including SF-1, WT1, DAX-1, and SOX9, that play key developmental roles in this process. Dose-dependent interactions among these genes are critical for sex determination and differentiation.

Animals↗
PubMed1997

Effects of day length and temperature on gonadal development, body mass, and fat depots in white-crowned sparrows, Zonotrichia leucophrys pugetensis.

We tested the effects of ambient temperature (5 degrees, 20 degrees, and 30 degrees) on photoperiodically induced reproductive functions in male and female white-crowned sparrows, Zonotrichia leucophrys pugetensis. Transfer from short days (9L 15D) to long days (16L 8D) resulted in rapid testicular growth and partial ovarian development in all three temperature treatments. There were no differences in sizes of testes and cloacal protuberance following 30 or 70 days of exposure to long days at the different temperatures. However, brood patch and follicular development were enhanced in females at 30 degrees compared with the 5 degrees and 20 degrees groups. Many of these females exposed to 30 degrees had large yolky follicles by Day 70. This enhancement was evident only when females were housed in the same room with males, however. Despite the effects of high temperature on ovarian development, there were no differences among groups in plasma levels of follicle-stimulating hormone or luteinizing hormone, suggesting that differential ovarian development may have been mediated by gonadal sensitivity to gonadotropins rather than by differential secretion of these hormones. We examined circulating levels of corticosterone (B) and both tri-iodothyronine (T3) and thyroxine (T4) as possible regulators of this differential ovarian sensitivity to gonadotropins. Plasma B levels showed transitory increases in males at 5 degrees and 20 degrees, but were suppressed in males at 30 degrees. Titers of B were not influenced by temperature treatments in females. Circulating T4 increased following photostimulation in both sexes, but this increase was reduced at 5 degrees. T3 concentrations in plasma were highly variable and not influenced by either photo-period or temperature in males, but were significantly lower in females exposed to 30 degrees by Day 70. Thus, B and T4 levels do not appear to help explain differential ovarian development, but circulating T3 levels cannot yet be excluded as a regulator of ovarian sensitivity to gonadotropins. Long days resulted in no change, or a gradual decrease, in body mass and fat deposit in males and females, and temperature regimes had no further effects on fattening or body mass. Thus, reproductive development under long days appears to be resistant to naturally relevant temperature extremes in male Z.l. pugetensis, whereas follicular development (i.e., yolk deposition in follicles leading to ovulation and onset of nesting) can be enhanced by high temperature. Reasons for the dimorphism in this response are unknown, but may be explained by the role of females in determining onset of final ovarian maturation and nesting in relation to favorable environmental conditions. In a second experiment, in which the sexes were isolated from one another, we determined the effects of the same treatments on.Z.I. pugetensis. Again there was no effect of temperature on photoperiodically induced testicular growth, and the enhancement of follicular development in females at 30 degrees was greatly reduced in the absence of males. We also continued this experiment up to 116 days of treatment to investigate effects on onset of photorefractoriness (spontaneous gonadal regression) and onset of prebasic moult. In both sexes it was clear that low temperature (5 degrees) retarded gonadal regression and high temperature (30 degrees) advanced it. Similarly, the prebasic moult score was greater at 30 degrees and less at 5 degrees in both sexes. There were no effects of temperature on plasma levels of LH at Day 116 of treatment, but plasma levels of T4 were higher in the 5 degrees group of both males and females sampled at Day 116. Clearly, the effects of temperature can have different effects on gonadal recrudescence, onset of breeding (yolk deposition), and termination of breeding. Whether these influences of temperature on reproductive function at different stages in the breeding cycle have different mechanisms remains to be determ

Adipose Tissue↗
PubMed2005

Temporal and spatial expression of liver receptor homologue-1 (LRH-1) during embryogenesis suggests a potential role in gonadal development.

Liver receptor homologue-1 (LRH-1), an orphan member of the nuclear receptor family highly expressed in adult mouse ovary, is closely related to steroidogenic factor 1 (SF-1), known to be important in gonadal formation. To analyze the potential role of LRH-1 in gonadal differentiation, we compared LRH-1 and SF-1 expression during mouse embryonic and postnatal development. LRH-1 expression was first detected in the urogenital ridge before sexual determination, in primordial germ cells and surrounding somatic cells; expression persisted after differentiation into testes and ovaries. Of interest, LRH-1 expression declined in the developing ovary and testis at embryonic day 15.5 but increased again just after birth in the ovary in granulosa cells and transiently in oocytes of developing follicles. By comparing and contrasting LRH and SF-1 expression with the two tissue-specific steroidogenic markers, cytochromes P450 aromatase and P450 17alpha-hydroxylase/17,20 lyase, we provide evidence for a potential role for LRH-1 in gonadal development, the initiation of folliculogenesis and regulation of estrogen biosynthesis within the ovary.

Animals↗
PubMed1997

Male-specific cell migration into the developing gonad.

BACKGROUND: The gene Sry acts as a developmental switch, initiating a pathway of gene activity that leads to the differentiation of testis rather than ovary from the indifferent gonad (genital ridge) in mammalian embryos. The early events following Sry expression include rapid changes in the topographical organization of cells in the XY gonad. To investigate the contribution of mesonephric cells to this process, gonads from wild-type mice (CD1), and mesonephroi from a transgenic strain ubiquitously expressing beta-galactosidase (ROSA26), were grafted together in vitro. After culture, organs were fixed and stained for beta-galactosidase activity to identify cells contributed from the mesonephros to the male or female gonad. RESULTS: Migration of mesonephric cells occurred into XY but not XX gonads from 11.5-16.5 days post coitum (dpc). Somatic cells contributed from the mesonephros were distinguished by their histological location and by available cell-specific markers. Some of the migrating cells were endothelial; a second population occupied positions circumscribing areas of condensing Sertoli cells; and a third population lay in close apposition to endothelial cells. CONCLUSIONS: OFFgration from the mesonephros to the gonad is male specific at this stage of development and depends on an active signal that requires the presence of a Y chromosome in the gonad. The signals that trigger migration operate over considerable distances and behave as chemoattractants. We suggest that migration of cells into the bipotential gonad may have a critical role in initiating the divergence of development towards the testis pathway.

Animals↗