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Female differentiation in the fetus is not default, has to be activated

New research suggests that the FOXL2 gene initiates the sex differentiation process, and when activated causes ovaries to develop.
By Ananth Baliga Follow @antbaliga Contact the Author   |   Jan. 31, 2014 at 10:01 AM
http://cdnph.upi.com/sv/em/i/UPI-2251391180489/2014/1/13911834842369/Female-differentiation-in-the-fetus-is-not-default-has-to-be-activated.jpg
PARIS, Jan. 31 (UPI) -- Female development in the fetus is activated by the FOXL2 gene, blocking male gene expression, meaning the default of sex of a fetus is not female.

Researchers at the INRA, in Paris, France, have identified the FOXL2 gene as responsible for female differentiation.

Females were long believed to be the "default" sex of a fetus, with a gene on the Y chromosome leading to male differentiation. But in some cases an XX fetus, programmed to be female, fails to develop ovaries and instead is born with male characteristics.

On analyzing the genes of such fetuses, researches identified the FOXL2 gene, which acts like a "defender of the ovary," silencing the male genes as the ovary develops and well into adulthood. These findings have been published in the journal Current Biology.

Using goat embryos, researchers silenced the FOXL2 gene and witnessed that XX fetuses developed testes instead of ovaries, explaining the development of male characteristics in XX fetuses.

The FOXL2 gene had previously been linked to premature menopause in young women. Techniques are being developed based on the goat model to treat certain types of infertility.


[INRA]
[Current Biology]

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