Ontogeny of expression of the genes for steroidogenic enzymes P450 side- chain cleavage, 3 beta-hydroxysteroid dehydrogenase, P450 17 alpha- hydroxylase/C17-20 lyase, and P450 aromatase in fetal mouse gonads

Abstract

It is well known that fetal androgens are required for male sexual differentiation, and it is thought that fetal ovaries are not steroidogenically active. However, molecular details, such as which steroidogenic enzymes are present in fetal testes and which enzymes are absent in fetal ovaries, have not been established. The pattern of expression of the genes that encode four of the steroidogenic enzymes necessary for androgen and estrogen production was examined during fetal development in mouse gonads. Messenger RNA (mRNA) expression for cholesterol side-chain cleavage (P450scc), 3 beta-hydroxysteroid dehydrogenase/delta 5-delta 4-isomerase (3 beta HSD), P450 17 alpha-hydroxylase/C17-20 lyase (P450c17), and P450 aromatase (P450arom) was determined before ovaries and testes were distinguishable (13 days postconception) and during sexual differentiation (15, 17, and 20 days postconception) using reverse transcriptase-polymerase chain reactions (RT-PCR). A PCR assay for Sry was used to determine gender on day 13. P450scc, 3 beta HSD, and P450c17 transcripts were detected at all ages in fetal testes, indicating that mRNAs for the steroidogenic enzymes that are required to convert cholesterol to androgens are present in the male gonad even before sexual differentiation. P450arom mRNA was detected in several fetal testes on day 17, but consistently observed on day 20. The expression of P450arom suggests the potential of fetal and neonatal testes to convert androgens to estrogens. In contrast, although 3 beta HSD mRNA was detected in several of the ovaries examined, the detection of P450scc, P450c17, and P450arom transcripts was rare. These data suggest that the absence of fetal ovarian steroid hormone production is the result of lack of expression of at least three of the steroidogenic enzymes, P450scc, P450c17, and P450arom.

Maternal obesity disturbs the postnatal development of gonocytes in the rat without impairment of testis structure at prepubertal age

“…Thus, Habert and colleagues have shown that homozygous inactivation of ERB increased the number of gonocytes by 50% in mice at 2 and 6 dpp due to an increase in the proliferation and decrease in apoptosis (Delbès et al 2004). Indeed, there are few data dealing with the production of estrogen in fetal and neonatal rodent testis (Habert & Picon 1984, Greco & Payne 1994, RouillerFabre et al 1998, Delbès et al 2004. These studies indicated that aromatase is expressed in Sertoli cells of fetal testis after the period of gonocyte proliferation (Greco & Payne 1994, Rouiller-Fabre et al 1998, which may explain no alterations in the Nv of gonocytes.…”

“…Indeed, there are few data dealing with the production of estrogen in fetal and neonatal rodent testis (Habert & Picon 1984, Greco & Payne 1994, RouillerFabre et al 1998, Delbès et al 2004. These studies indicated that aromatase is expressed in Sertoli cells of fetal testis after the period of gonocyte proliferation (Greco & Payne 1994, Rouiller-Fabre et al 1998, which may explain no alterations in the Nv of gonocytes. However, our data indicate that postnatal aromatase activity probably was affected by MO.…”

Aromatase expression in the ovary: Hormonal and molecular regulation

“…In many species, ovaries acquire the enzymatic capacity to produce estrogen during embryonic life as determined by the capacity of fetal ovaries to convert radiolabeled androgen to estrone and estradiol [6][7][8] or by the amplification of aromatase cDNA by PCR [9]. Aromatase expression in fetal ovaries is extremely low; although it can be increased by treatment with an analog of cAMP but not by follicle stimulating hormone (FSH) [8,10].…”

Isolation of chicken homolog of the FOXL2 gene and comparison of its expression patterns with those of aromatase during ovarian development

“…In the mouse, aromatase expression starts after birth, when the ovary is already well differentiated (Greco and Payne, 1994), whereas Foxl2 expression begins as early as 13.5 dpc in the developing female gonads (Loffler et al, 2003, Pannetier et al, 2003. On the other hand, FoxL2 in the red-eared slider turtle is up-regulated at the female promoting temperature in the differentiating gonads during the temperature sensitive period (TSD; Loffler et al, 2003), whereas no dimorphism in aromatase expression in the adrenal-kidney-gonad complex has been found at female or male promoting temperature during the TSD (Murdock and Wibbels, 2003).…”