Abstract

In therian mammals, genomic imprinting, typically via methylation of either the paternal or maternal allele, results in a monoallelic and parent-of-origin expression pattern of a subset of genes. Careful maintenance of the expression of these “imprinted” genes is crucial to mammalian development, with misexpression in humans or model organisms evidenced in a series of prenatal, neonatal, and postnatal growth and developmental phenotypes that impact adult metabolic health. Imprinted genes exert their effects in utero via both placental and embryonic tissues, with their dysregulation leading to fetal growth defects and abnormal control of placental resources. In the neonatal and postnatal period, they govern the feeding, thermoregulation, and social behaviors in both the offspring and the mother. Furthermore, metabolic syndrome in adulthood is a consequence of gene–environment interactions via altered imprinted gene expression in the postnatal period, demonstrating the importance of tightly controlled growth and development in early life.

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