Scientists thought for years that the ovaries and testes are fully developed, stable organs that cannot change their structure and function in mature mammals. However, more recent studies have shown that a gene called Foxl2 is active throughout life to prevent ovary cells from becoming more like the Sertoli cells present in the testes. Similarly, a gene called Dmrt1 keeps Sertoli cells from becoming more like ovary cells after birth. Scientists don’t yet know all the details about how Dmrt1 prevents testes from becoming more ovary-like. For example, do genes that help testes develop in the embryo (which include two genes called Sox8 and Sox9) play a role in maintaining the adult testes? Barrionuevo, Hurtado, Kim et al. have now genetically engineered adult male mice to lack the Sox8 and Sox9 genes. The Sertoli cells in the testes of these mice gradually lost their key characteristics and ultimately died. During this process, the testes cells took on certain characteristics that made them more ovary-like for example, the ovary-maintaining Foxl2 gene was activated in the Sertoli cells. Eventually, the structures in the testes that produce sperm degenerate and are replaced by empty space in the genetically engineered mice. This happens because the Sox8 and Sox9 genes control the production of proteins that maintain these structures. In addition, these genes also protect the Sertoli cells from self-destructing, and the testes-maintaining Dmrt1 gene is not active when Sox8 and Sox9 are missing. More studies are now needed to determine how Sox8 and Sox9 work with Dmrt1 to maintain the testes.
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