In 1990, researchers made headlines when they uncovered the identity of this gene, which they called SRY. Just by itself, this gene can switch the gonad from ovarian to testicular development. For example, XX individuals who carry a fragment of the Y chromosome that contains SRY develop as males.
By the turn of the millennium, however, the idea of femaleness being a passive default option had been toppled by the discovery of genes that actively promote ovarian development and suppress the testicular programme—such as one called WNT4. XY individuals with extra copies of this gene can develop atypical genitals and gonads, and a rudimentary uterus and Fallopian tubes. In 2011, researchers showed that if another key ovarian gene, RSPO1, is not working normally, it causes XX people to develop an ovotestis—a gonad with areas of both ovarian and testicular development.
These discoveries have pointed to a complex process of sex determination, in which the identity of the gonad emerges from a contest between two opposing networks of gene activity. Changes in the activity or amounts of molecules (such as WNT4) in the networks can tip the balance towards or away from the sex seemingly spelled out by the chromosomes. "It has been, in a sense, a philosophical change in our way of looking at sex; that it's a balance," says Eric Vilain, a clinician and the director of the Center for Gender-Based Biology at the University of California, Los Angeles. "It's more of a systems-biology view of the world of sex."