Ed Yong has a fascinating article on the behavior of a gene called SRY. It is located on the Y chromosome, and is pivotal in making an embryo develop into a male. But what about studies of Swyer syndrome, in which a child inherits the father's Y chromosome, but does not develop into a male? Children with Swyer syndrome are born and raised female, but do not become fertile at puberty. However, their fathers may have an identical SRY gene, and obviously were male. What makes the difference? The the gene does not always cause maleness, as it has a rather weak mechanism that is dependent on conditions being just so. Michael Weiss from Case Western Reserve University presented the research, and Melissa Wilson-Sayres from the University of Berkeley compares the gene to a dimmer switch as opposed to an off-on switch -or analog vs. digital.
That’s very strange. There are many master genes that play pivotal roles in our development, controlling the growth of eyes, limbs and more. If these genes don’t work properly, the results could be catastrophic. So, they ought to be exceptionally stable—enforcing the status quo in the face of all but the most severe mutations or environmental conditions. It should take much more than a 2-fold difference in activity to change what they do. “We’d expect to see factors of 50-fold or more,” says Weiss. “These master switches are meant to be rigorously locked in. They’re not meant to be this tenuous.”
So, why does SRY operate from such a wobbly position? Why have a set-up that could so easily lead to infertility? For the variety, says Weiss. He thinks that the vagaries of SRY leads to a wide variety within developing testes, and a wide variation in the amount of testosterone they produce. This hormone influences our behaviour, including many aspects of our social lives. So, at the risk of the occasional infertile XY female, a precariously-set master switch leads to a broad spectrum of male brains, which may make for a better-functioning society. “You can’t have all alpha-males in a group,” suggests Weiss.
It’s a fairly speculative idea, and Wilson-Sayres isn’t convinced. She says that the far simpler explanation is that the Y-chromsome is especially prone to picking up mutations with weak harmful effects.