Germs' fate as sperm or egg in vertebrates is decided by a single modifier, a gene called foxl3, at least in medaka fish.
In medaka, also called Japanese rice fish, foxl3 suppresses the mutation of germs into sperm, the researchers conclude in the online pre-print edition of the journal Science.
The study was conducted by researchers from Japan's National Institute for Basic Biology, the Institute for Integrative Bioscience and Kyushu University.
Researchers isolated the foxl3 gene and observed that, without it, female medaka fish produce sperm inside of their ovaries, and a small amount of eggs and that sperm is capable of successfully fertilizing eggs.
Regardless of the conditions surrounding the germ cells' medaka's gonadal environment, researchers confirmed that the firm the females produce is capable of successfully fertilizing eggs and producing offspring. All of this surprised the National Institute for Basic Biology's Toshiya Nishimura.
"That this sexual switch present in the Germ Cells is independent of the body's sex is an entirely new finding," said Nishimura.
It was already known that germ cells in vertebrates can go either way, sperm or eggs, but no one knew that there is a "switch mechanism" that determines their fate, stated Minoru Tanaka, associate professor at the National Institute for Basic Biology.
"Our result indicates that once the decision is made the germ cells have the ability to go all the way to the end," said Tanaka. "I believe it is of very large significance that this mechanism has been found."
Back in 2009, another member of the FOX gene family, foxl2, was shown to suppress the masculinity of mice. By completely removing the foxl2 gene from the ovaries of females, the mice, three weeks later, had transitioned into males and produced testosterone.
"The major finding is that females must actively suppress the male pathway inside the ovary," said Geneticist Mathias Treier back in 2009. "Here is a gene that is not located on the sex chromosome that makes you stay female."
Before that, researchers transitioned mice ovaries into testes by shutting off the estrogen receptors. The newly male mice didn't produce testosterone, however.
