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Controlling sex ratios

I formerly thought that when a tendency to produce the two sexes in equal numbers was advantageous to the species, it would follow from natural selection, but I now see that the whole problem is so intricate that it is safer to leave its solution for the future. -- Charles Darwin in Descent of Man
This week, I will discuss recent papers that shed light on the evolution of genes that control sex ratios in insects (fruit flies) and mammals (mice). John Dennehy recently discussed Hamilton's 1967 paper, "Extraordinary Sex Ratios." (Yes, Hamilton, as in Hamilton's r.) See also the last paragraph of this post, on the surprisingly sophisticated adjustment of offspring sex ratios by fig-pollinating moths.

As Darwin was starting to recognize, natural selection doesn't depend on whether a trait is advantageous to the species. If the effects of an allele (a particular DNA sequence) cause it to become more common, relative to alternative alleles that compete for the same space on a chromosome, then it will become more common, whatever the effects on the species as a whole. As Richard Dawkins famously pointed out, natural selection acts as if each gene were "selfish."

In particular, alleles that increase the chance of having male, rather than female, offspring will tend to become more common when males are rare, and vice versa. This is because each individual of the minority sex will generally have disproportionately high genetic representation in the next generation. If a population has one female and ten males, for example, every member of the next generation will be descended from that female, whereas the chance of being descended from any individual male is only 10%. The parents of girls born in China today are more likely to become grandparents than the parents of boys, although this could be affected by international migration.

So that's why natural selection often leads to a 50:50 sex ratio. But deviations from this ratio do occur, as Hamilton noted. This leads to two questions. What is the ultimate (evolutionary) reason for different sex ratios? And the proximate (mechanistic) question: to what extent can individuals actually control the sex ratio of their offspring, and how?

Two papers by Yun Tao and colleagues on control of sex ratio in fruit flies were just published in PLoS Biology. Because this is an open-access journal and because PLoS includes a well-written summary, by Patrick Ferree and Daniel Barbash, I will only discuss the main points.
In fruitflies, as in humans, females have two X chromosomes, whereas males have one Y chromosome and one X. Each parent contributes a copy of one of its sex chromosomes to each offspring. If males had an equal chance of contributing and X or a Y (as is approximately true in humans), then half of the offspring would be male and half would be female. But sexual equality is threatened by Dox (Distorter on X), an allele on the X chromosome that promotes its own transmission (rather than the Y chromosome) from XY fathers to their offspring. Because the offspring always get an X chromosome from their XX mother, this selfish gene leads to a preponderance of female (XX) offspring. All else being equal, it would tend to spread, leading to an all-female species and likely extinction. This could happen. This may have happened in other species. There is nothing in evolution that guarantees the survival of a species; most species that ever lived are extinct.

But in this case, Tao et al. also found another gene, which they named Nmy (not much yang), that suppresses the Y-killing activity of Dox.
The left side of the diagram is what they think happened after Dox evolved but before Nmy. The RNA or protein product of Dox kills Y chromosomes, so only female-producing sperm with the X chromosome survive. The right hand side of the diagram shows how suppression works today. Messenger RNA from Nmy binds to messenger RNA from Dox. The cell's defenses against double-stranded RNA (typically viruses) degrade it. But for RNA from Dox to bind with RNA from Nmy, they would have to be complementary. An amazing coincidence? More likely, Nmy is derived from Dox by duplication, a common source of evolutionary innovation.

Also this week, Elissa Cameron and colleagues published "Experimental alteration of litter sex ratios in a mammal" in Proceedings of the Royal Society.

It has been suggested that mothers with enough resources to produce larger-than-average offspring would have more grandchildren if they produce more sons than daughters. This assumes that big males have more opportunities to reproduce but female reproduction depends less on size, which may be true of many mammals. But how much control do mothers have over the sex ratio of their offspring?

To find out, they induced a decrease in the nutritional status of mice, using a steroid hormone that lowers glucose levels in the blood. They measured actual change in glucose during pregnancy and the sex ratio of the baby mice. Mothers whose glucose increased (almost all steroid-free) had more sons, while those whose glucose decreased (mostly steroid-treated) had more daughters. From their graph, it looks like the percentages were about 60% vs. 40%.

Of course, the steroid treatment could have had a wide variety of effects. For example, an earlier study they cite found that the same hormone reduced increases in male-biased sex ratio that were blamed on stress. But this study, and other results cited (including one on diabetes) suggest that blood glucose may be a key player in controlling sex ratio in at least some mammals.

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