Abstract
The crucial event in mammalian sexual differentiation occurs at the embryonic stage of sex determination, when the bipotential gonads differentiate as either testes or ovaries, according to the sex chromosome constitution of the embryo, XY or XX, respectively. Once differentiated, testes produce sexual hormones that induce the subsequent differentiation of the male reproductive tract. On the other hand, the lack of masculinizing hormones in XX embryos permits the formation of the female reproductive tract. It was long assumed that once the gonad is differentiated, this developmental decision is irreversible. However, several findings in the last decade have shown that this is not the case and that a continuous sex maintenance is needed. Deletion of Foxl2 in the adult ovary lead to ovary-to-testis transdifferentiation and deletion of either Dmrt1 or Sox9/Sox8 in the adult testis induces the opposite process. In both cases, mutant gonads were genetically reprogrammed, showing that both the male program in ovaries and the female program in testes must be actively repressed throughout the individual’s life. In addition to these transcription factors, other genes and molecular pathways have also been shown to be involved in this antagonism. The aim of this review is to provide an overview of the genetic basis of sex maintenance once the gonad is already differentiated.
Highlights
The crucial event in mammalian sexual differentiation occurs at the embryonic stage of sex determination, when the bipotential gonads differentiate as either testes or ovaries, according to the sex chromosome constitution of the embryo, XY or XX, respectively
Using lineage-specific transgenic mice, Jameson et al (2012) showed that the supporting cells appeared to acquire their sex-specific fates by embryonic day 11.5 (E11.5), whereas the sex-specific differentiation of both interstitial/stromal cells and germ cells began at E12.5, when the supporting cells had almost completed their process of differentiation
XY Cell sex reversal could explained by functional failure of sexThe assumption that gonadal differentiation is irreversible was motivated the specific factors at the sex determination stage, suggesting that alterations were by never fact that most cases of XXHowever, or XY sexcases reversal could be explainedbetween by functional failure produced at later stages
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Further experiments using transgenic mice expressing the testis determining gene, Sry, to trace the fate of supporting cells showed that XX and XY supporting cell lines have a common precursor [8,9]. This “common progenitor identity” hypothesis was later confirmed in studies using transcriptomic profiling [10,11,12,13]. Sertoli cells promote the differentiation of the steroidogenic Leydig cells and prevent germ cells from meiosis entry In mice, all these events are almost completed within 24–48 h after sex determination.
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