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Authors: Paul Raeburn
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undersupplied for the next, risking its life or her own. The male, on the other hand, wants to extract as much of the mother’s energy and resources as he can for his offspring. Or, as Haig puts it, “Maternal genes have a substantial interest in the mother’s well-being and survival. Paternal genes favor greater allocation of maternal time and effort to their particular child.”
The stage is now set for competition. The male and female do whatever they can to advance their competing strategies. But how do they do that? How can a father manipulate the mother to extract maximum resources for the child? And how can a mother conserve her resources and make sure that doesn’t happen? Haig’s insight was that imprinted genes are the weapons that males and females use to pursue their competing strategies. The imprints that mothers and fathers put on the genes turn them off or on as needed to pursue these strategies.
The gene’s “imprint” is stamped on it by the parent, and that imprint affects the expression of the gene in the offspring. The genes that are expressed when inherited from fathers tend to encourage more growth in the fetus. They push the fetus to demand more resources from its mother while it’s in the womb—to suck up as many maternal resources as possible, pursuing the father’s competitive strategy. Genes that are expressed when inherited from mothers tend to slow that growth, so the mother can conserve resources for subsequent children.
* * *
Haig’s theory was meant to explain not only what Surani had found but also what others found as they began to explore the implications of Surani’s research. While Surani can claim credit for discovering the phenomenon of imprinting, he didn’t know which genes were imprinted or precisely what each of them did. It took about a decade for researchers to discover the first imprinted gene. That was the work of Elizabeth Robertson, then in the Department of Genetics and Development at Columbia University and now at the University of Oxford in England. She was investigating normal growth and development in mice by inactivating, or knocking out, certain genes to see what effect that would have on developing embryos. In a paper published in Cell in 1991, Robertson and her colleagues reported an unusual discovery regarding a gene called Igf2 , which is responsible for the production of something called insulin-like growth factor II, or IGF-II. When the researchers knocked out the gene in mouse mothers, nothing happened. The offspring were normal. That meant the gene must have little or no role in the offspring’s development. But when Robertson knocked it out in mouse fathers , the embryos grew to only about 60 percent of the size of their normal counterparts. When the gene came from a father—and only when it came from a father—it was clearly essential for growth.
This fit nicely with Haig’s theory. The paternal gene enabled the fetus to draw more nutrients from its mother, a crucial part of the father’s mating strategy. This was critical experimental evidence of the competition between mothers and fathers. Other researchers quickly followed with the discovery of other imprinted genes, and the genes that came from the fathers encouraged fetal growth, as Haig theorized. Taken to the extreme, this strategy had a serious drawback: if the fetus extracted too much from its mother, she would die, and so would the fetus.
The new discoveries also began to reveal mothers’ powerful counterweapon: genes that are maternally stamped fight back against the male strategy, encouraging the fetus to draw only the nutrients it needs to survive, not as many as it can. Mothers put their stamp on a gene that counters the growth boost by Igf2 . It’s called Igf2r , and it’s the gene for what’s called the IGF-II receptor. In order for the male’s IGF-II to work, it must plug into the IGF-II receptor. If the female controls the receptor, she can moderate the
The stage is now set for competition. The male and female do whatever they can to advance their competing strategies. But how do they do that? How can a father manipulate the mother to extract maximum resources for the child? And how can a mother conserve her resources and make sure that doesn’t happen? Haig’s insight was that imprinted genes are the weapons that males and females use to pursue their competing strategies. The imprints that mothers and fathers put on the genes turn them off or on as needed to pursue these strategies.
The gene’s “imprint” is stamped on it by the parent, and that imprint affects the expression of the gene in the offspring. The genes that are expressed when inherited from fathers tend to encourage more growth in the fetus. They push the fetus to demand more resources from its mother while it’s in the womb—to suck up as many maternal resources as possible, pursuing the father’s competitive strategy. Genes that are expressed when inherited from mothers tend to slow that growth, so the mother can conserve resources for subsequent children.
* * *
Haig’s theory was meant to explain not only what Surani had found but also what others found as they began to explore the implications of Surani’s research. While Surani can claim credit for discovering the phenomenon of imprinting, he didn’t know which genes were imprinted or precisely what each of them did. It took about a decade for researchers to discover the first imprinted gene. That was the work of Elizabeth Robertson, then in the Department of Genetics and Development at Columbia University and now at the University of Oxford in England. She was investigating normal growth and development in mice by inactivating, or knocking out, certain genes to see what effect that would have on developing embryos. In a paper published in Cell in 1991, Robertson and her colleagues reported an unusual discovery regarding a gene called Igf2 , which is responsible for the production of something called insulin-like growth factor II, or IGF-II. When the researchers knocked out the gene in mouse mothers, nothing happened. The offspring were normal. That meant the gene must have little or no role in the offspring’s development. But when Robertson knocked it out in mouse fathers , the embryos grew to only about 60 percent of the size of their normal counterparts. When the gene came from a father—and only when it came from a father—it was clearly essential for growth.
This fit nicely with Haig’s theory. The paternal gene enabled the fetus to draw more nutrients from its mother, a crucial part of the father’s mating strategy. This was critical experimental evidence of the competition between mothers and fathers. Other researchers quickly followed with the discovery of other imprinted genes, and the genes that came from the fathers encouraged fetal growth, as Haig theorized. Taken to the extreme, this strategy had a serious drawback: if the fetus extracted too much from its mother, she would die, and so would the fetus.
The new discoveries also began to reveal mothers’ powerful counterweapon: genes that are maternally stamped fight back against the male strategy, encouraging the fetus to draw only the nutrients it needs to survive, not as many as it can. Mothers put their stamp on a gene that counters the growth boost by Igf2 . It’s called Igf2r , and it’s the gene for what’s called the IGF-II receptor. In order for the male’s IGF-II to work, it must plug into the IGF-II receptor. If the female controls the receptor, she can moderate the
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