Epigenetics, and in particular imprinted genes, play a critical role in the development and function of the placenta, which in turn, plays a central role in the regulation of fetal growth and development. A unique characteristic of imprinted genes is their expression from only one allele, maternal or paternal, dependent on parent-of-origin. This unique expression pattern may have arisen as a mechanism to control the flow of nutrients from the mother to the fetus/offspring, with maternally expressed imprinted genes reducing the flow of resources and paternally expressed genes increasing resources to the fetus. As a result, any epigenetic deregulation affecting this balance can result in fetal growth abnormalities. In humans, imprinting- associated disorders such as Beckwith-Wiedemann and Angelman syndrome, support the role of imprinted genes in fetal growth. Similarly, assisted reproductive technologies in animals have been shown to affect the epigenome of the early embryo as well as expression of imprinted genes. Their role in disorders such as intrauterine growth restriction (IUGR) appears to be more complex in that imprinted gene expression can be seen as both causative and protective of fetal growth restriction. This protective or compensatory effect needs to be more fully explored.
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