Genomic imprinting, growth control and the allocation of nutritional resources: consequences for postnatal life

Abstract

Purpose of review: Genes subject to genomic imprinting are predominantly expressed from one of the two parental chromosomes, are often clustered in the genome, and their activity and repression are epigenetically regulated. The role of imprinted genes in growth control has been apparent since the discovery of imprinting in the early 1980s.

Recent findings: Drawing from studies in the mouse, we propose three distinct classes of imprinted genes - those expressed, imprinted and acting predominantly within the placenta, those with no associated foetal growth effects that act postnatally to regulate metabolic processes, and those expressed in the embryo and placenta that programme the development of organs participating in metabolic processes. Members of this latter class may interact in functional networks regulating the interaction between the mother and the foetus, affecting generalized foetal well-being, growth and organ development; they may also coordinately regulate the development of particular organ systems.

Summary: The mono-allelic behaviour and sensitivity to changes in regional epigenetic states renders imprinted genes adaptable and vulnerable; in all cases, their perturbed dosage can compromise prenatal and/or postnatal control of nutritional resources. This finding has implications for understanding the relationships between prenatal events and diseases later in life.