Did Human Pregnancy Evolve Because of an Infection?
Scientists may know why our babies advance so much in the womb.
Photo by iStockphoto/Thinkstock.
If someone were to tell you that roughly 100 million years ago, our ancestors were infected by parasitic DNA, which copied and pasted itself throughout their genomes—and that this was linked to the evolution of modern human pregnancy—you might assume they were channeling early L. Ron Hubbard.
But this week, in the prestigious journal Nature Genetics, researchers provide evidence for such a theory. Seeking to explain how our ancestors developed a more advanced kind of gestation—including the ability to carry fetuses in the womb until they reached a more developed state—scientists studied the uterine cells of three contemporary mammals. Specifically, they compared opossums (whose young develop largely in pouches) to armadillos and humans (whose offspring spend more time in the womb). They concluded that rogue DNA, which probably arrived by way of a virus or bug, was associated with wild new horizons in baby-making.
For all our cultural obsession with fertility, from Beyonce’s bump to fiftysomethings giving birth, little is known about the long-ago cellular events that set us on track toward our present styles of pregnancy.
Here’s what we do know: Today’s mammals all descend from a common ancestor. But when it comes to reproduction, we are quite the motley bunch. Some, called monotremes, lay eggs. These include the duck-billed platypus and spiny anteater. Others, called marsupials, undergo brief pregnancies, giving birth (in the case of the opossum) after roughly two weeks. At that point, opossum pups are just strong enough to climb up into their mama’s pouches where they suckle and continue to develop before entering the wide world.
Still others, the placental mammals, which are considered more advanced, tend to make pregnancy last. Armadillos, for instance, carry their progeny in the womb for roughly 60 to 120 days. We do it, of course, for around nine months. During that time, we nourish our fetuses by way of a long-lasting placenta, which invades the uterine wall. We respond to soaring levels of estrogen and progesterone, pump higher volumes of blood, and modify our immune responses in part so that we don’t reject our fetuses, which then develop more extensively before birth. Put another way: “an opossum hardly knows it’s pregnant,” according to Vincent Lynch of Yale, first author of the new work in Nature Genetics. By which he means that these animals don’t undergo the kind of sustained, physiological upheaval that we do. Armadillos’ bodies, on the other hand, are more aware of their condition—and not only because some carry identical quadruplets each time. (Humans, of course, are all too conscious of sore boobs and swollen ankles, notwithstanding the outliers on I Didn’t Know I Was Pregnant.)
For years, researchers have puzzled over why some animals evolved the ability to carry offspring internally until they reached a more developed state. In a scientific tour de force, Lynch and his colleagues took a muscular swing at that question. They began with endometrial cells from the opossum, the armadillo, and the human. Using a sequencing approach that allowed for large-scale analysis, they considered the genes that were turned on in each of these animals during pregnancy. Then they homed in on differences between the marsupial opossum and the placental mammals, the armadillo and the human. Remarkably, they found that new stretches of DNA, called transposons, were scattered throughout the armadillo and human cells. These transposons appeared to act as light switches for genes that got turned on only in the uteruses of the more advanced animals.
Scientists suspect that this rogue DNA may have gotten in through an infection, in part because there’s at least one example of blood-sucking parasites potentially carrying transposons into animals. But once inside, the new DNA got busy reproducing. “It’s like they’re a parasite in your gut except they’re a parasite in your DNA and all they care about is making more copies of themselves,” said Lynch. Researchers already knew that a transposon, called MER20, helped turn on a gene, called prolactin, that is important during pregnancy. But the new work suggests that the transposon’s role might have been much broader—that thousands of copies of MER20, which spread throughout the animals’ DNA, might have helped to regulate hundreds of genes that respond to estrogen and progesterone and could have helped the womb sustain a longer and more complex pregnancy. In other words, the DNA invasion might have moved us, to some degree, not toward pups in a pouch but babes in a Baby Bjorn.
Of course, modern pregnancy is a complex beast. Researchers don’t believe the transposon incursion was sufficient, by itself, to explain the shift toward pregnancy in placental mammals like us. For one thing, the current work doesn’t address the evolution of the placenta itself. Nor does it zero in on immune changes that have long been viewed as necessary for more sustained gestation. “You clearly need to alert the immune system that that thing in the uterus” that only shares half the mother’s DNA “is not a parasite and is not to be rejected,” as Lynch himself points out. Large gaps remain in these parts of the story. But the invasion of rogue DNA may be one crazy—and important—twist in the tale of modern human pregnancy for which we ought to be oddly grateful.
Amanda Schaffer is a science and medical columnist for Slate.