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Authors: Paul Raeburn
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greedy nutrient-seeking of IGF-II. Denise P. Barlow and colleagues at the Research Institute of Molecular Pathology in Vienna discovered that Haig’s theory held once again. Igf2r , as expected, was also imprinted—but in the opposite direction. The receptor gene was active only when it came from the mother. When the Igf2r gene is knocked out in fathers, nothing happens. But when the Igf2r gene is knocked out in female mice, the offspring grow too big and die before birth.
Haig published a paper about this fascinating competition with a title worthy of Sherlock Holmes: “Genomic Imprinting and the Strange Case of the Insulin-like Growth Factor II Receptor.” In it, Haig writes, with appropriate Sherlockian flourish, “Surely, it is no coincidence that IGF-II and its type 2 receptor are oppositely imprinted.” For Haig, this was an exciting confirmation of his theory. The two genes enabled the parents to battle over the size of their offspring, each of them advancing his or her own evolutionary goals. To those who might be critical of his theory, Haig chose Holmes himself to respond: “It is an old maxim of mine that when you have excluded the impossible, whatever remains, however improbable, must be the truth.”
Humans have counterparts to these genes, and when this system goes awry, the consequences can be devastating. Suppose, for example, a mother’s and father’s copies of IGF2 (scientists capitalize the names of human genes and use lowercase letters to indicate nonhuman genes) are both mistakenly turned on—the mother’s isn’t turned off as it should be. Or suppose the fertilized egg accidentally gets two copies of the father’s turned-on gene. The fetus then gets a double dose of growth genes. This leads to a condition called Beckwith-Wiedemann syndrome, in which children have birth weights more than 50 percent above normal. And the opposite mistake can occur. If both genes are silenced, the fetus doesn’t draw on its mother’s resources the way it should, and it is born below normal weight.
“It’s a tug-of-war,” Haig said. “You’ve got these two sides tugging on the rope. They’re not shifting much—it’s just a little bit one way or the other. And they come to depend on each other, on the other side holding the rope. If you get a mutation in an imprinted gene, you get a really pathological outcome. One side has let go of the rope.”
Until recently, genes subject to this gender division were thought to be rare, numbering perhaps a hundred or so out of the estimated 25,000 human genes. But Haig and his colleague Catherine Dulac, a Harvard molecular biologist, used a different method to find imprinted genes and concluded that there could be more than a thousand of them. Some critics have questioned this result, arguing that the study had flaws and that imprinted genes are not as common as Haig and Dulac claim. But whether or not that’s the case, it’s clear that this genomic battle of the sexes is not a rare phenomenon that plays out in isolated corners of the human genome—it’s far more widespread.
Whatever the actual number of imprinted genes turns out to be, it is already clear that many of them are expressed only in the brain, where they can affect behavior in many ways. Indeed, maternal and paternal genes battle for control in the brains of every one of us. As Catherine Dulac told me, “We know we get conflicting advice from mom and dad. Here it’s in the genome—it’s in your own brain! So you can’t escape mom and dad fighting over what you’re supposed to do.” But these imprinted genes are not expressed in all parts of the brain. That raises an interesting question. Research has shown that imprinting errors can affect a fetus’s growth and even threaten its life. Could errors in imprinted brain genes be linked to mental illness?
Christopher Badcock of the London School of Economics and Bernard Crespi of Simon Fraser University in British Columbia think so. They
Haig published a paper about this fascinating competition with a title worthy of Sherlock Holmes: “Genomic Imprinting and the Strange Case of the Insulin-like Growth Factor II Receptor.” In it, Haig writes, with appropriate Sherlockian flourish, “Surely, it is no coincidence that IGF-II and its type 2 receptor are oppositely imprinted.” For Haig, this was an exciting confirmation of his theory. The two genes enabled the parents to battle over the size of their offspring, each of them advancing his or her own evolutionary goals. To those who might be critical of his theory, Haig chose Holmes himself to respond: “It is an old maxim of mine that when you have excluded the impossible, whatever remains, however improbable, must be the truth.”
Humans have counterparts to these genes, and when this system goes awry, the consequences can be devastating. Suppose, for example, a mother’s and father’s copies of IGF2 (scientists capitalize the names of human genes and use lowercase letters to indicate nonhuman genes) are both mistakenly turned on—the mother’s isn’t turned off as it should be. Or suppose the fertilized egg accidentally gets two copies of the father’s turned-on gene. The fetus then gets a double dose of growth genes. This leads to a condition called Beckwith-Wiedemann syndrome, in which children have birth weights more than 50 percent above normal. And the opposite mistake can occur. If both genes are silenced, the fetus doesn’t draw on its mother’s resources the way it should, and it is born below normal weight.
“It’s a tug-of-war,” Haig said. “You’ve got these two sides tugging on the rope. They’re not shifting much—it’s just a little bit one way or the other. And they come to depend on each other, on the other side holding the rope. If you get a mutation in an imprinted gene, you get a really pathological outcome. One side has let go of the rope.”
Until recently, genes subject to this gender division were thought to be rare, numbering perhaps a hundred or so out of the estimated 25,000 human genes. But Haig and his colleague Catherine Dulac, a Harvard molecular biologist, used a different method to find imprinted genes and concluded that there could be more than a thousand of them. Some critics have questioned this result, arguing that the study had flaws and that imprinted genes are not as common as Haig and Dulac claim. But whether or not that’s the case, it’s clear that this genomic battle of the sexes is not a rare phenomenon that plays out in isolated corners of the human genome—it’s far more widespread.
Whatever the actual number of imprinted genes turns out to be, it is already clear that many of them are expressed only in the brain, where they can affect behavior in many ways. Indeed, maternal and paternal genes battle for control in the brains of every one of us. As Catherine Dulac told me, “We know we get conflicting advice from mom and dad. Here it’s in the genome—it’s in your own brain! So you can’t escape mom and dad fighting over what you’re supposed to do.” But these imprinted genes are not expressed in all parts of the brain. That raises an interesting question. Research has shown that imprinting errors can affect a fetus’s growth and even threaten its life. Could errors in imprinted brain genes be linked to mental illness?
Christopher Badcock of the London School of Economics and Bernard Crespi of Simon Fraser University in British Columbia think so. They
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