Sexual dimorphism in the neonatal gonad. Acta Paediatr 1999; Suppl 428:23-30. Stockholm. ISSN 0803-5326The neonatal gonad has two distinct forms (i.e., is sexually dimorphic), as judged by morphological and endocrine characteristics. The dimorphic process begins early in embryogenesis. It is well established by the time of birth, by which time the genital ridge has developed into either a testis or an ovary. The mechanisms involved in sex determination involve the Y chromosome, autosomal genes, transcription factors and possibly other unidentified control networks. This review paper describes the morphological changes that occur and the endocrine functions in the developing gonads. It highlights a number of important differences in fetal and neonatal gonadal function. The testis has early histological definition, several determining genes, delayed germ cell maturation, early autonomous steroid secretion, luteinizing hormone (LH) receptor and steroid enzyme expression, high fetal testicular testosterone content, prominent postnatal Leydig and Sertoli cells and high postnatal serum testosterone levels. The ovary has a prolonged monomorphic state, probably one determining gene, germ cells in early meiotic arrest, delayed expression of LH receptor and aromatase, low ovarian oestradiol content, prominent postnatal follicles and low postnatal serum oestradiol levels. 0 Dimorphism, endocrine function, gonads, morphology, ovary, testis During early embryogenesis, the mammalian gonad is monomorphic or indifferent in morphological appearance. The neonatal gonad, however, is sexually dimorphic (i.e., exhibits two distinct forms) in both morphological and endocrine characteristics. This sexual dimorphism of the neonatal gonad is the result of a multitude of genetic factors that effect the switch from a monomorphic to a dimorphic state in early gestation.
The genetic switchThe simplistic model that invokes the pivotal role of the Y chromosome in gonadal sexual dimorphism and, hence, sex determination, is shown in Fig. 1. The SRY gene on the short arm of the Y chromosome has been well established, by molecular genetic and clinicopathological studies, as a major player in testis determination (1). Furthermore, autosomal genes are also involved in sex determination, as evidenced by the study of sex reversal syndromes (2-4). The use of targeted gene disruption technology has highlighted the role of transcription factors, such as WT-1 ( 5 ) , SF-1 (6) and LIM-1 (7), in genital ridge development prior to the dimorphic stage.However, disruption of these Y-linked and autosomal genes cannot account for all cases of XY sex reversal, which indicates that additional control networks remain to be identified.
Genital ridgeMonomorphic gonad J Ovary XY