(Find Part 1 here)
Okay, so Ms. Washington’s twins have two daddies. It’s just tabloid-fodder, right?. But reading it (hey, it’s my job!) I saw a kind of grandeur in this tale: a window into our evolutionary past. After all, routine gestation of a single child is a late development; most mammals carry littermates, often with different baby-daddies. These offspring compete for scarce maternal resources during and after the pregnancy — a competition that may explain the origin of maternal and paternal imprinting of chromosomes.
Here’s the thing: in evolutionary terms, the best interests of the mother and the best interests of the father are not always aligned. During a pregnancy and over her lifetime, a mother aims to produce as many healthy offspring as possible, which means protecting her own health and distributing her resources evenly, to maximize the chances of multiple babies in multiple litters. What with monogamy being a new idea – maybe that’s why we’re not better at it! — fathers back in the day were relatively unconcerned about the long-term health of the mother. Their mandate was to promote the success of their own offspring, even if it came at the expense of the gestating, caretaking parent (why do you think they call it MAN-date, anyway?). Competition would be particularly intense among littermates – if one father could find a way to get his offspring a disproportionate amount of maternal resources, his genes would thrive at the expense of others. In evolutionary terms, a good day at the office.
Conflict Theory, a school of evolutionary thought espoused by David Haig among others, looks at the consequences of these dueling agendas. Genetic changes that increase or speed-up growth would be favored – when they came from the father. Genetic changes that restrict or delay growth would be favored – when they came from the mother. Evolution would become a see-saw affair.
Let’s take the example of IGF-1, which promotes growth in multiple tissues in utero. Dad wants to make sure his kids are not the runts of the litter; mom wants to look a bit less like a beached whale. Mutations over time alternately increase and decrease the rate of production of IGF-1. Then one day a mutation occurs affecting methylation patterns that shuts down the maternally-inherited allele entirely – imprinting. In the war between the sexes, it is the evolutionary equivalent of the discovery of gunpowder.
Davor Solter first provided evidence of something like imprinting when he discovered in 1984 that proper mouse development required one male and one female set of chromosomes. Use all paternal genes and you get an underdeveloped fetus and too much placental tissue – like a molar pregnancy, which results from an empty egg and two sperm. Molar pregnancies are dangerous because of their unrestricted, highly invasive growth – just what you might have predicted from conflict theory. Maternal-only fetuses look more like mice but are small, and lack supportive tissue.
The same logic can be used to predict which parent’s genes are over- or under-expressed in syndromes involving imprinted alleles. Beckwith-Wiedemann, an overgrowth disorder, can be caused by a double dose of paternal genes. The diminutive Russel-Silver baby? – a double dose from mom. Recently, a novel variant was found that is associated with the development of type II diabetes, but only when the allele is inherited from…drumroll please….dad.
So if you think the superfecund Ms. Washington is a sign of the times, think again. Men may not have realized until now that such a thing was possible, but their genes have known it forever. And if you think your genes are making you fat – kids, I’m begging you – blame your Dad.
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