A standoff continues between genes inherited from mother and father in the womb, revealing that the “battle of the sexes” begins before birth, scientists have found.
The fetus uses a hormonal signal to control its nutrient supply from the placenta, scientists from the University of Cambridge said. As he grows up he has to communicate his need for more nutrients to his mother, receiving the nutrition through the blood vessels of the placenta.
In a study on genetically modified embryonic mice, published today in Developmental Cell, scientists found that the fetus produces the signal, known as IGF2, to encourage the growth of blood vessels in the placenta, and that it involves a “tug of war” between the genes inherited from the mother and the father.
While only the copy of IGF2 inherited from the father is active, a gene expressed by the mother acts to counteract the additional demands for food made by IGF2.
Lead author Dr Miguel Constancia said: “One theory about imprinted genes is that the genes expressed by the father are greedy and selfish. They want to extract as many resources as possible from the mother.
“But the genes expressed by the mother act as countermeasures to balance these demands.”
“In our study, the father’s gene determines the fetus’s need for larger blood vessels and more nutrients, while the mother’s gene in the placenta tries to control the amount of food it provides.
“There’s a tug-of-war going on, a genome-level battle of the sexes.”
Dr Ionel Sandovici, first author of the article, said: “As it grows in the womb, the fetus needs the nourishment of its mother and healthy blood vessels in the placenta are essential. to help him get the right amount of nutrients he needs.
“We have identified a way the fetus uses to communicate with the placenta to cause these blood vessels to expand properly.
“When this communication is interrupted, the blood vessels do not develop properly and the baby will have difficulty getting all the food he needs. “
The team found that IGF2 reaches the placenta through the umbilical cord, with IGF2 levels in humans gradually increasing from 29 weeks to term.
With too much IGF2, there will be excessive growth, while too little is associated with poor growth, both of which are linked to health complications.
The response of placental blood vessels to IGF2 in mice is mediated by the IGF2R protein. The genes that produce IGF2 and IGF2R are “imprinted,” with molecular switches that identify their parental origin, and these can turn them on or off.
Only the copy of IGF2 inherited from the father is active, while only the copy of IGF2R inherited from the mother is active.
The team said the study would help improve understanding of how the fetus, placenta, and mother communicate during pregnancy, which could lead to new ways of using drugs to normalize levels of IGF2.