In 2009, Henriette Uhlenhaut from the European Molecular Biology Laboratory engaged in a study that revealed this early change is not necessarily a permanent one.  Henriette conducted a study using mice that had been genetically altered so that FOXL2 could be “turned off” via a drug called Tamoxifen.  Henriette found that once FOXL2 had been deleted, a landslide of genetic changes took place.  Within three weeks the female ovaries had become testes and the female hormone estrogen had been outflanked by the male hormone testosterone.  Henriette found that these female mice with XX chromosomes were now producing the same levels of testosterone as the male mice with XY chromosomes.  The female mice only fell short of the males in their inability to reproduce.

    The study showed that in females, FOXL2 is a gatekeeper gene which keeps the male forming DMRT1 gene in submission and found that one gene will always be dominate and the other will be submissive.  When the FOXL2 gene is “turned off” or repressed, the male DMRT1 becomes dominant causing the female mice to become genetically male.

    Clinton Matson from the University of Minnesota recently conducted a similar study using male mice.  As with FOXL2 study, Clinton found if the DMRT1 gene is deleted or suppressed, FOXL2 will become dominant causing the male testes to become ovaries (see image above) and estrogen to surge through the bloodstream while testosterone levels dropped.

    Mathias Treier, the leader of Uhlenhaut’s FOXL2 study, applauds Clinton’s discoveries, having said “When we tried to publish our paper that ovaries can be reprogrammed to testis, we were fighting an uphill battle against an old dogma that mammalian sex determination is final.  It is gratifying for us to see that the reverse is also possible.”

    These studies offer a deep insight into how environmental factors may be causing females to be born who possess XY chromosomes and men who are born with XX chromosomes as well as hope that in future, such mutations can be corrected.

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