New research reveals a genetic tug-of-war within the developing fetus
A fascinating new study unveils a prenatal rivalry: genes inherited from the father vie with maternal genes over fetal nutrition, beginning even before birth.
Published Monday in Development Cell, this investigation reveals a genetic struggle within the womb. The conflict ignites when the developing offspring signals its nutritional needs via a hormone – IGF2.
The study delves into the reasons behind impaired fetal growth, affecting 10-15% of pregnancies. Often, this involves deficient placental blood vessel development. The researchers employed genetically modified mice, whose biology closely mirrors that of humans.
The researchers discovered that paternal genes, upon receiving the IGF2 signal, trigger placental blood vessel expansion to enhance nutrient delivery. Conversely, maternal genes strive to limit this expansion.
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Excessive IGF2 results in overgrowth; insufficient levels (due to maternal gene dominance) lead to restricted growth. Both extremes pose health risks.
“A prevailing theory on imprinted genes posits that paternally expressed genes are self-serving, aiming to maximize resource extraction from the mother. In contrast, maternal genes act as regulatory countermeasures,” explained lead researcher Miguel Constancia.
The father’s genetic contribution drives the fetus’s demand for enlarged blood vessels and increased nutrient supply, while the mother’s genes within the placenta attempt to regulate nutrient provision. This represents a fundamental genomic conflict, a battle of the sexes at the molecular level.
However, this genetic competition is ultimately beneficial: the opposing forces maintain nutritional equilibrium, ensuring adequate fetal nourishment.
These findings will significantly enhance our comprehension of the complex communication network between the fetus, placenta, and mother during gestation. This could lead to refined methods of assessing fetal IGF2 levels and potentially, the development of therapies to regulate these levels.
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