Natural selection can favor genes that allow children to grow up healthy. But in order to grow up healthy, they need nurturing from their mothers, both before and after birth. If a baby’s development puts a strain on a mother, she may end up having fewer children. That means she may spread fewer copies of her genes to later generations . That creates conditions in which natural selection may also genes that allow mothers to restrain their children. Our particular way of having kids puts genes in conflict.
I have an article in tomorrow’s New York Times on these conflicting genes, focusing on the visionary work of David Haig of Harvard University. As I explain in the article, Haig first wrote about his theory in the early 1990s. He made a number of predictions about pregnancy and fetal growth, many of which have only been tested in recent years. Many of them bolster his argument.
In articles such as this one, I usually have to struggle over which examples to include and which to leave out. Sometimes extemely cool ones demand a lot of explanation which would swamp the whole piece. In this case, I had to leave out a couple striking examples of how genes in conflict may create some of the most mysterious birth disorders around.
As I explain in the article, sometimes a mother’s or father’s copy of a gene is silenced. (This is sometimes called gene imprinting.) Haig argues that gene imprinting evolves to undercut the effect of genes from the other parent. A gene that stimulates growth in fetuses puts a strain on the mother. So the mother’s copy of the gene in the fetus is silenced, reducing the growth of the fetus. Imprinted genes are often linked to diseases, because only a single gene has to do a particular job, without backup from the other parent’s gene. And the effects of these disorders can reveal the evolutionary forces that drive the evolution of gene imprinting.
An estimated one in 25,000 babies is born with Prader-Willi syndrome, which causes them to show almost no interest in feeding. Prader-Willi syndrome has been linked to a set of imprinted genes. The syndrome may be triggered if a mutation deletes the father’s copies of these genes. So it may be that these are genes that drive the growth of babies by causing them to nurse more. Mothers hold the children back by silencing their copies of the genes.
By age three, children with Prader-Willi syndrome undergo a baffling change. They develop an insatiable appetite and an obsession with finding food. Prader-Willi can lead to severe obesity. Haig argues that this shift is also the result of genetic conflict. One clue is that it occurs right around the time when children are weaned. Weaning marks a major potential conflict for children and their parent. If a child can nurse longer, it may be more likley to thrive. But if a mother can wean her child, she doesn’t have to sacrifice more energy to make breast milk. Nursing also acts as a contraceptive, so putting a child onto solid food can make it possible for a mother to get pregnant again. The effects of Prader-Willi suggest that paternal genes are driving children to resist weaning. Mothers silence those genes to counteract that resistance.
Another enigmatic disorder is known as Angelman syndrome. Children with Angelman syndrome suffer from a number of symptoms, including retardation. But they’re most distinctive for abundant laughter and endless happiness. Angelman syndrome is caused by the disruption of imprinted genes. It’s the mother’s genes that are disrupted in Angelman syndrome, as opposed to the father’s in Prader-Willi.
What does it mean if disabling maternal genes causes children to laugh and be happy? In a paper in press, Lawrence Wilkinson and his colleagues at Cambridge University argue that babies use these sort of signals to get more attention from their mothers. So the genes that normally prevent Angelman syndrome may normally act as a brake on those signals.
These are speculations, but fascinating ones, and ones that line up with more thoroughly studied examples of genes in conflict. Fortunately, what can’t fit in the paper can always fit in the blog.
[Update 3/14: a little tinkering to clear up the beginning, per a commenter's request]