The other event involves Pi-RNA pathway genes, such as Miwi2, Mili,and Tdrd1, 5, and 9, required for transposon silencing. Two critical events follow NANOS2 expression: One is the induction of DNMT3L, which is an essential component of methyltransferase acting with DNMT3A and 3B by which the male-type DNA methylation status, including imprinting genes and retrotransposons, is established. Male germ cells stop proliferation and enter G0 arrest at around E14.5 and start to express male-specific genes required for preparation as prospermatogonia. The earliest clear sex difference observed in germ cells is associated with the cell cycle status and is characterized by the expression of 2 sex-specific factors, NANOS2 in male germ cells and STRA8 in female germ cells. At least in humans and mice, germ cell sex is determined by environmental factors supplied by somatic cells. Indeed, XY PGCs are capable of becoming oocytes upon sex reversal induced in the somatic environment, and germ cells derived from XY ES cells in chimeric mice can produce oocytes and contribute to the next generation. However, in embryonic PGCs, there is no evidence of any chromosomal difference that affects sexual differentiation, although there may be some quantitative differences in the gene expression level such as transcripts from the X chromosome. Therefore, testis- or ovary-specific gene expression can be observed at E12.5 in somatic cells. On the contrary, in the absence of SRY in XX gonads, genes normally repressed by the Srygene cascade, such as Wnt4, Foxl2, and R-Spondin, are upregulated to form an ovary.
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A series of gene cascades leads to the expression of the so-called male specifying factors SOX9, FGF9, and CYP26B1 to promote testis formation in XY gonads. Somatic sex determination begins around E10.5, which is initiated by the expression of SRY from the Y chromosome. Sexual differentiation of germ cells begins after primordial germ cells (PGCs) specified in the early embryo enter and colonize embryonic gonads, which are composed of somatic cells (Fig. Introduction: Overview of Germ Cell Sexual Differentiation Key Messages: The important message is that although testis-specific factors secreted from the testis are considered to include male-inducing factors for germ cells, this may not be the case, and the male-inducing factor, if it exists, also exists in the ovary. There should be signals required for germ cells to enter a male pathway. However, this has not been confirmed in an in vitro culture system. This may be true in vivo because germ cells enter a male pathway if they do not receive these signals even in the ovary.
However, what about male? If these factors are female determinants, their absence may result in the induction of spermatogonia. From the viewpoint of germ cells, an independent experiment identified SMAD4 and STRA8, which are directly downstream of BMP and RA, respectively, acting in germ cells as female determinants. Therefore, these 2 signals may be referred to as oogonia inducers. However, researchers realized that a big, open question remained: What somatic cell signals actually induce the sexual differentiation of germ cells and what is the sex determinant in germ cells? Summary: In vitro experiments demonstrated that 2 somatic signals (BMP and RA) act directly on germ cells to induce oogonia. Therefore, the sex of germ cells is thought to follow the sex of somatic cells once determined. Basically, the sex of individual somatic cells and germ cells matches. This is because the issue of sexual differentiation has generally been considered a theme of somatic cells to make a testis or ovary.
However, the induction mechanism has not received much attention until relatively recently. Background: Whether to produce sperm or eggs is the most basic and important choice from the perspective of germ cell development and differentiation.
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