The battles of the sexes begins in the womb: study

Scientists now say life’s proverbial “battle of the sexes” actually begins in the womb — with a father and mother’s genes fighting over how much nutrition a fetus should receive.

University of Cambridge researchers made the findings while investigating why some babies struggle to grow properly in the womb, according to their new study published Monday in the scientific journal Developmental Cell.

The scientists used genetically engineered mice — who are biologically similar to humans — during their research.

A fetus receives its nourishment via blood vessels in the placenta — a special organ containing cells from both the baby and its mother. Therefore, healthy blood vessels are essential for the fetus to get the correct amount of nutrients that it needs.

During pregnancy, a fetus sends a signal known as IGF2 from the placenta through the umbilical cord to prompt the correct expansion of these blood vessels.

Interestingly, the scientists discovered that the father’s genes try to expand the blood vessels in a bid to suck up more nutrients. The mother’s genes fight back, trying to restrict the expansion of the blood vessels and slow down the nutritional intake.

The fight between the genes is actually a good thing — as they are actually balancing one another out, making sure the fetus receives the correct nutritional intake. Lead study author Miguel Constância said “paternally expressed genes are greedy and selfish … They want to extract the most resources as possible from the mother. But maternally expressed genes act as countermeasures to balance these demands.”
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However, the fight between the genes is actually a good thing — they balance one another out to create a healthy baby.

Lead study author Miguel Constância told SWNS that “paternally expressed genes are greedy and selfish.”

“They want to extract the most resources as possible from the mother — but maternally expressed genes act as countermeasures to balance these demands,” he explained.

Too much IGF2 (caused by the dominance of the paternal gene) is linked with too much growth, while not enough IGF2 (a dominance of the maternal gene) is associated with too little growth.

Up to 15% of babies grow poorly in the womb, and abnormally large or small babies are more likely to suffer or even die at birth.

Too much IGF2 (caused by the dominance of the paternal gene) is linked with too much growth. Not enough IGF2 (a dominance of the maternal gene) is associated with too little growth.
Too much IGF2 (caused by the dominance of the paternal gene) is linked with too much growth. Not enough IGF2 (a dominance of the maternal gene) is associated with too little growth.
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Constância continued, “In our study, the father’s gene drives the fetus’ demands for larger blood vessels and more nutrients, while the mother’s gene in the placenta tries to control how much nourishment she provides.”

He surmised: “There’s a tug-of-war taking place, a battle of the sexes at the level of the genome.”

Ionel Sandovici, the study’s co-author, added: “We’ve known for some time that IGF2 promotes the growth of the organs where it is produced.”

“In this study, we’ve shown that IGF2 also acts like a classical hormone – it’s produced by the fetus, goes into the fetal blood, through the umbilical cord and to the placenta, where it acts.”

Dr Miguel Constancia, states that "paternally-expressed genes are greedy and selfish. They want to extract the most resources as possible from the mother. But maternally-expressed genes act as countermeasures to balance these demands.”
Constância said, “There’s a tug-of-war taking place, a battle of the sexes at the level of the genome.”
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The researchers believe that their findings will help people understand how the fetus, the placenta and the mother communicate with each other during pregnancy.

This could then lead to ways of measuring the levels of IGF2 in the fetus and finding ways to use medication to normalize these levels so that the unborn baby receives the correct nutritional intake during pregnancy.