The Riddle of Gender - Deborah Rudacille [167]
In the sober language of science, Demir and Dickson describe the effects of their experiment in a June 2005 paper published in the prestigious journal Cell.
“Forcing female splicing in the male results in a loss of male courtship behavior and orientation, confirming that male specific splicing of fru is indeed essential for male behavior. More dramatically, females in which fru is spliced in the male mode behave as if they were males: they court other females. Thus, male-specific splicing of fru is both necessary and sufficient to specify male courtship behavior and sexual orientation. A complex innate behavior is thus specified by the innate of a single gene.”
So what, some people might say. Fruit flies aren’t human beings, and just because tweaking a single gene turns a fruit fly community into West Hollywood doesn’t mean that human sexual orientation and gender identity are biologically based. True enough, although drosophila are one of the most popular model systems used by scientists to study genetics and much has been learned from the manipulation of the fruit fly genome. But just to satisfy those who don’t see the relevance of fruit fly genetics to human behavior, let’s turn to some studies in other species more like us, fellow mammals. Mice, for example.
Around the time I was finishing the research for this book, researchers at UCLA discovered that testosterone might not be quite the all-powerful force scientists had assumed when it comes to prenatal sexual differentiation. Throughout this book I have repeated the central dogma of sex research, that maleness is the result of the surge of testosterone midway through the second month of pregnancy. Before the newly formed testicles begin flooding the developing embryo with testosterone, the embryo is androgynous; without that all-important gush of testosterone, it will develop “by default” in the female direction. I mentioned that many female biologists object to this notion of female being the “default” sex, and point out that even if we don’t know exactly what causes an embryo to develop in the female direction, something must be happening. It turns out that they may be right.
Eric Vilain, chief of medical genetics at UCLA, has used DNA microarray analysis to blow a giant hole in the prevailing theory that steroid hormones produced by the gonads are responsible for sex differences in neural and behavioral development. By chopping up embryonic mouse brains, purifying and amplifying their DNA, and measuring the expression of various proteins, Vilain and colleagues identified over fifty genes expressed differently in the brains of male and female mouse embryos before the gonads begin producing any hormones at all.
As the researchers pointed out in an October 2003 paper published in Molecular Brain Research, their results “suggest that there are functional differences between male and female brains which occur independently from hormonal influence. Moreover, these differentially expressed genes are good candidates for a role in brain sexual differentiation and sexual behavior.”
Vilain’s findings attracted a good deal of attention in the media, as did the gender-queer fruit fly study. But unlike Demir and Dickinson, the fruit fly researchers, Vilain didn’t hesitate to connect the dots between mouse brains and human ones. Vilain is a clinician as well as a researcher, and has long worked with intersex children and their families. The knowledge he has gleaned from his work in both the lab and the clinic have convinced him that defining maleness and femaleness from a biological standpoint is a very complex undertaking. “There is no one biological parameter that clearly defines sex,” he says. Nonetheless, his research has shown that the sexual differentiation of the brain begins very early in development,