The gonads have an important role in germ cell development, converting the bipotential cells into gametogonia. The germ cells are bipotential in that prior to migrating to the gonads, they are capable of forming either spermatogonia or oogonia. The specification into either female or male fates for the organism itself also depends on the development of the gonads, which have yet to differentiate into ether ovaries or testes. In the mouse, somatic sex determination (i.e. determination of either female or male gonads) begins at embryonic day 10.5 in mice, but is not finalised until day 12.5. Male somatic cell specification involves the Y-chromosome specific Sry gene, which regulates the specification of
Sertoli cells and
Leydig cells. Without the specification of those cells, the gonad formation is regulated by the X-chromosomes, forming the ovaries. After the fate of the gonads is finalised, the sex specification of the germ cells occurs at 12.5-15.5 days. Sex specification of the germ cells requires the repression of pluripotency and relies on the communication between the somatic cells of the gonads and germ cells. The mechanisms for male and female differentiation are markedly different, since a population of sperm producing spermatogonia are retained throughout development and into adult life, unlike oogonia which only produce oocyte in utero. When the germ cells reach the gonads, they undergo proliferation via mitosis and at 13.5 days of rat development they begin to undergo meiosis in the ovary but arrested at the mitotic stage in the testes. In the ovary, after
mitosis, the gametogonium undergo
meiosis, which is initiated by intrinsic competence factor
DazL and extrinsic
retinoic acid, excreted by the
mesonephros. Retinoic acid is the major factor in meiosis, upregulating genes including ‘‘Stra8’‘, ‘‘
Dmc1’‘ and ‘‘
Sycp3’‘, which all have a role in meiosis. The male germ cells are protected from external signalling, like retinoic acid from the mesonephros, by the Leydig and Sertoli cells. ==Spermatogonium==