Gonadal sex differentiation and expression of Sox9a2, Dmrt1, and Foxl2 in Oryzias luzonensis

Oryzias luzonensis is closely related to the medaka, O. latipes. The sex of both species is determined by an XX‐XY system. However, the testis determining gene (DMY/Dmrt1bY) found in O. latipes does not exist in O. luzonensis. Instead, a different gene is thought to act as a testis determining gene. In this study, we focused the gonadal sex differentiation process in O. luzonensis under different testis determining gene. First, we observed the gonadal development of O. luzonensis histologically. We then analyzed the expression of Sox9a2/Sox9b, Dmrt1, and Foxl2 during early development. Our results suggest that the sexual differentiation of germ cells in O. luzonensis is initiated later than in O. latipes. However, the timing of the sexual differentiation of the supporting cell linage is similar between the species. genesis 47:289–299, 2009. © 2009 Wiley‐Liss, Inc.     

Sex determination in humans

In mammals, the Y chromosome induces testis formation and thus male sexual development; in the absence of a Y chromosome, gonads differentiate into ovaries and female development ensues. Molecular genetic studies have identified the Y-located testis determining gene SRY as well as autosomal and X-linked genes necessary for gonadal development. The phenotypes resulting from mutation of these genes, together with their patterns of expression, provide the basis for establishing a hierachy of genes and their interactions in the mammalian sex determination pathway.     

Genetic mechanisms underlying male sex determination in mammals

Genetic control of gonadal development proceeds through either the male or female molecular pathways, driving bipotential gonadal anlage differentiation into a testis or ovary. Antagonistic interactions between the 2 pathways determine the gonadal sex. Essentially sex determination is the enhancement of one of the 2 pathways according to genetic sex. Initially, Sry with other factors upregulatesSox9 expression in XY individuals. Afterwards the expression ofSox9 is maintained by a positive feedback loop withFgf9 and prostaglandin D₂ as well as by autoregulative ability of Sox9. If these factors reach high concentrations, then Sox9 and/or Fgf9 may inhibit the female pathway. Surprisingly, splicing, nuclear transport, and extramatrix proteins may be involved in sex determination. The male sex determination pathway switches on the expression of genes driving Sertoli cell differentiation. Sertoli cells orchestrate testicular differentiation. In the absence of Sry, the predomination of the female pathway results in the realization of a robust genetic program that drives ovarian differentiation.