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PubMed1999

Proliferative and steroidogenic effects of follicle-stimulating hormone during chick embryo gonadal development.

The aim of this study was to evaluate the in vitro effect of human follicle-stimulating hormone (hFSH) on cellular proliferation and steroid hormone secretion in the left ovary, the right ovary, and the testis of the chick embryo. Gonads from 8- to 18-day-old chick embryo were cultured in a defined medium during 60 h under basal and hFSH-stimulated conditions (0.5 IU/ml of culture medium). At the end of the culture, the incorporation of ¿(3)Hthymidine and the total number of cells were measured to estimate gonadal cell proliferation. The secretion of 17beta-estradiol and testosterone in the culture medium was radioimmunologically assayed in order to evaluate the steroidogenic function of the cultured gonadal cells. The response to hFSH stimulation was observed in the left ovary, the right ovary, and the testis from the 8-day-old chick embryo. In the left ovary, cellular proliferation was not augmented by hFSH in the 8-, 10-, and 13-day-old chick embryo; meanwhile, the proliferative stimulus of hFSH was observed in the 15- and 18-day-old embryos. In the same ovary, 17beta-estradiol and testosterone secretion were stimulated after hFSH treatment at all evaluated stages (8-18 days of chick embryo development). In the right ovary, an increment in proliferation and steroidogenesis was induced by hFSH in the 8-, 10-, and 13-day-old chick embryo. Afterward, the right gonad did not respond to hFSH. Testis cells displayed hFSH response as an increment in cell proliferation at all embryonic ages (8-18 days of chick embryo development). There was a transient lack of response to hFSH in testosterone secretion at 10 and 13 days of development. The in vitro effect of hFSH on cell proliferation and steroid hormone secretion changed in the ovary and the testis according to the age of the embryo. These changes could be attributed to the growth of the left ovary and the testis and the regression of the right ovary. Probably, paracrine factors modulated the gonadotropin effect on the target cells during embryonic development of chick embryo gonads.

Animals↗
PubMed2001

Normal gonadal development in mice lacking GPBOX, a homeobox protein expressed in germ cells at the onset of sexual dimorphism.

Gpbox is a paired-like homeobox gene that colocalizes with two other members of the family, PsxI and Pem, on the proximal portion of the mouse X chromosome. Gpbox is expressed in the extraembryonic placenta and within the germ cells of the embryonic gonad. Beginning with the onset of sexual dimorphism (embryonic day [E]11.5 to 12.5), GPBOX transcripts accumulate faster in female than in male germ cells but disappear later in embryogenesis (E16) and have not been reported in adult tissues. To investigate the function of Gpbox, mouse cell lines lacking GPBOX were established using targeted mutagenesis in embryonic stem cells. Both homozygous Gpbox null female and hemizygous Gpbox null male mice were fertile and reproduced normally. Additionally, the development of male and female gonads in the null background was indistinguishable from that observed in normal littermates. The lack of an obvious phenotype raises the possibility that another member of this homeobox gene family provides the absent Gpbox function.

Animals↗
PubMed1998

Role of Ahch in gonadal development and gametogenesis.

Ahch (also known as Dax1) encodes a transcription factor that has been implicated in sex determination and gonadal differentiation. Mutations in human AHC cause X-linked, adrenal hypoplasia congenita (AHC) and hypogonadotropic hypogonadism (HH). Duplication of the Xp21 dosage-sensitive sex reversal (DSS) region, which contains the Ahch locus, and transgenic overexpression of Ahch cause male-to-female sex reversal. Using Cre-mediated disruption of Ahch, we have generated a mouse model of AHC-HH that allows the function of Ahch to be examined in both males and females. Although Ahch has been postulated to function as an ovarian determination gene, the loss of Ahch function in females does not affect ovarian development or fertility. Ahch is instead essential for the maintenance of spermatogenesis. Lack of Ahch causes progressive degeneration of the testicular germinal epithelium independent of abnormalities in gonadotropin and testosterone production and results in male sterility. Ahch is thus not an ovarian determining gene, but rather has a critical role in spermatogenesis.

Adrenal Glands↗
PubMed1989

Fibroblast growth factor and the control of pituitary and gonad development and function.

Evidence from in vitro studies support the concept that growth factors could be involved in the development, maturation and function of endocrine organs. Included among the growth factors which are known to influence endocrine cell proliferation and differentiation is the fibroblast growth factor (FGF), which controls the proliferation, differentiation, and other functions of mesodermal- and neuroectodermal-derived cells. Its modulator, transforming growth factor beta (TGF beta), which determines the positive or negative direction of the effects of FGF, may play a role as well. In this review, we present a speculative view of how FGF in the pituitary gland, and both FGF and TGF beta in the gonads could influence the development and function of these organs through regulating mechanisms involving paracrine and autocrine control of cell proliferation and differentiation.

Aging↗
PubMed1984

Role of thyroid and testicular hormones in the regulation of basal metabolic rate, gonad development, and body weight of spotted munia, Lonchura punctulata.

Normal saline, L-thyroxine (L-T4, 0.5 micrograms/bird/day), and testosterone (100 micrograms/bird/day) were administered separately to intact, thyroidectomized, and castrated spotted munia over a 30-day period and the effects on basal metabolic rate (BMR), gonads, and body weight were recorded. Thyroidectomy and castration decreased the BMR. L-Thyroxine increased the BMR of intact and thyroidectomized but not of the castrated birds. Testosterone had no effect on BMR of either the intact or of the operated birds. L-Thyroxine and testosterone both had no effect on regressing gonads but inhibited thyroidectomy-induced testicular development. Body weight increased in intact, testosterone-treated birds, and in thyroidectomized and castrated spotted munia. L-Thyroxine inhibited body weight gain only in thyroidectomized birds. It is suggested that the physiological actions of L-T4 and testosterone depend on the gonadal status, thyroid activity, and nature of the thyroid-gonad relationship.

Animals↗
PubMed1995

Suprachiasmatic nucleus and photoperiodic regulation of gonadal development in the Siberian hamster, Phodopus sungorus.

Photoregressed Siberian hamsters exposed at 19 days of age to constant light for 24 h manifested increased testicular development 16 days later. Hamsters that sustained lesions of the suprachiasmatic nucleus (SCN) 3 days after the light pulse had significantly heavier gonads than did sham-operated animals or hamsters pinealectomized at 19 days of age. Enhanced reproductive development after SCN ablation is not due solely to lesion-induced elimination of melatonin secretion. SCN neural activity beginning 3 days after the light pulse is not necessary for light-induced gonadal growth.

Animals↗
PubMed1997

Porcine Dax-1 gene: isolation and expression during gonadal development.

The identification of XY females carrying a duplication of a region of the X chromosome (Xp21) led to the hypothesis that a double dose of a gene in the duplicated region causes sex reversal (DSS; dosage sensitive sex reversal). A gene isolated from this region, named DAX-1 (DSS-AHC critical region on the X), encodes a new member of the nuclear hormone receptor family. Here, we describe the isolation of porcine Dax-1 and the analysis of its pattern of expression both during foetal development and in several adult tissues. Dax-1 is expressed in the adrenals, the pituitary gland and the gonads at various stages of differentiation. In gonads, Dax-1 expression starts between 21 and 23 days post coitum in both XX and XY urogenital ridges then continues to be expressed until adult age. The expression in these tissues indicates the involvement of DAX-1 in the development and the function of the reproductive system at multiple levels.

Amino Acid Sequence↗
PubMed2001

Estradiol and incubation temperature modulate regulation of steroidogenic factor 1 in the developing gonad of the red-eared slider turtle.

Red-eared slider turtles are genetically bipotential for sex determination, with incubation temperature of the egg determining gonadal sex. At higher incubation temperatures, females are produced, possibly due to increased biosynthesis of estrogen. Exogenous estrogen causes the formation of ovaries, and prevention of estrogen biosynthesis results in the development of testes. In mammals, steroidogenic factor 1 (SF-1) regulates most genes required for estrogen biosynthesis from cholesterol. In mammals as well as red-eared slider turtles, SF-1 is differentially expressed in males and females during gonadogenesis. To examine a possible role for SF-1 in temperature-dependent sex determination, we assayed its expression in red-eared slider turtles after treatments that alter sex development during gonadogenesis of the wild-type organism. We examined gonadal SF-1 expression in embryos 1) incubating at three different temperatures, 2) after treating eggs with estrogen at a male-producing temperature, and 3) after inhibition of estrogen biosynthesis at a female-producing temperature. Our findings suggest that both temperature and estrogen lie upstream of SF-1 in a sex-determining regulatory hierarchy in red-eared slider turtles and that estrogen directly or indirectly modulates the regulation of SF-1 expression.

Animals↗
PubMed1986

Gonadal development of the chick embryo following microsurgically caused agenesis of the mesonephros and using interspecific quail-chick chimaeras.

Mesonephric agenesis was achieved by microsurgical excision of the left Wolffian duct and the underlying intermediate mesoderm of different regions between somites 16 and 23 in chickens after 50-52 h of incubation (stage 14 HH). Quail-chick chimaeras were produced by transplantation of corresponding quail tissue in the region of somites 18-21. A morphometrical analysis of the mesonephric and gonadal area in cross sections shows that the intermediate mesoderm from somites 16 to 23 develops into the mesonephros. A partial agenesis of the mesonephros brought about by removal of the intermediate mesoderm at the level of somites 18 to 21 at stage 14 leads to a mean reduction of the gonadal volume of 37.8% compared to the volume of the untreated side at stage 30. Transplantation of quail intermediate mesoderm in this region of the excision results in development of a hybrid mesonephros. Consequently, the gonads are invaded and colonized by quail cells mobilized from mesonephric corpuscles examined at stage 30, 35 and 36. These results are discussed in terms of the origin of the gonadal stroma during this developmental period; they show that in the region from the third to the sixth segment the ventromedial part of the differentiating mesonephros participates in the contribution of stromal cells to the gonad.

Animals↗