title: Functional genomics and sexual differentiation in amphibians.
abstract: In Xenopus laevis the basic mechanisms underlying sexual differentiation were investigated by determining time courses of sexual steroids and their corresponding receptors during complete larval development from egg to juveniles. Androgens as well as estradiol (E2) are derived from maternal origin and accumulate in hatching tadpoles. Sexual steroid contents decreased rapidly after hatching and rose again at the end of metamorphosis indicating endogenous production. In parallel the mRNA expression for corresponding androgen (AR) and estrogen receptors (ER) was measured by means of semiquantitative RT-PCR. Both receptor mRNAs increased dramatically just after hatching and decreased only moderately until end of metamorphosis. In female juveniles E2 and ER-mRNA levels were higher compared with males. Treatment by exogenous E2 elevated both, ER- and AR-mRNA, indicating stimulatory functions of E2 for gene expression of both receptors. Effects on sexual differentiation during larval development were achieved by treatment with E2 and the antiandrogen cyproterone acetate both causing feminization, the antiestrogen tamoxifen resulting in neutralization, and the androgens, methyltestosterone and dihydrotestosterone, but not testosterone, leading to masculinization. The data presented are in accordance with further recent findings and suggest a new hypothesis for functional genomics in sexual differentiation of amphibians.
authors.affiliation: Department of Inland Fisheries, Leibniz-Institute of Freshwater Ecology, Müggelseedamm 310, 12587, Berlin, Germany.
authors.forename: Christian
authors.initials: C
authors.lastname: Bögi
authors.forename: Gregor
authors.initials: G
authors.lastname: Levy
authors.forename: Ilka
authors.initials: I
authors.lastname: Lutz
authors.forename: Werner
authors.initials: W
authors.lastname: Kloas
mesh_terms: D000728:Androgens / Q000494:pharmacology; D000818:Animals; D018931:Antineoplastic Agents, Hormonal / Q000494:pharmacology; D017931:DNA Primers / Q000737:chemistry; D013196:Dihydrotestosterone / Q000494:pharmacology; D004958:Estradiol / Q000494:pharmacology; D004965:Estrogen Antagonists / Q000494:pharmacology; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000235:genetics*; D023281:Genomics; D012739:Gonadal Steroid Hormones / Q000494:pharmacology; D008297:Male; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011944:Receptors, Androgen / Q000235:genetics* / Q000378:metabolism; D011960:Receptors, Estrogen / Q000235:genetics* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012733:Sex Differentiation / Q000502:physiology*; D013629:Tamoxifen / Q000494:pharmacology; D013739:Testosterone / Q000494:pharmacology; D014982:Xenopus laevis / Q000502:physiology*
chemical_list: D000728:Androgens; D018931:Antineoplastic Agents, Hormonal; D017931:DNA Primers; D004965:Estrogen Antagonists; D012739:Gonadal Steroid Hormones; D012333:RNA, Messenger; D011944:Receptors, Androgen; D011960:Receptors, Estrogen; D013196:Dihydrotestosterone; D013629:Tamoxifen; D013739:Testosterone; D004958:Estradiol