Integrated studies on embryonic survival and prenatal development in swine

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Prenatal programming of variability in postnatal growth performance in swine as an economically important aspect of "phenotypic plasticity". Lifetime production potential in livestock species is ultimately controlled by the interaction between the highly selected genotype of an animal and its environment. These environmental factors are operative in both the prenatal and postnatal periods. It is becoming clear that lifetime growth potential may be limited by key events occurring early in embryonic and fetal development. Programming of early embryonic development is a complex process that is initially controlled by maternally derived regulators in the cytoplasm of the fertilized oocyte, and is then controlled by the expression of the uniquely reconstituted embryonic genome. However, expression of the embryonic genome is subject to epigenetic (environmental) regulation, mediated by "imprinted" genes that are only expressed from either the maternal or the paternal allele. The mechanism of gene imprinting involves DNA methylation, and there is evidence that this process can be altered by maternal nutrition. An unequivocal role of "imprinted genes" in the regulation of placental development, fetal demand for maternal nutrients and resulting fetal intrauterine growth retardation (IUGR), has not been established in the pig. A primary objective of our NSERC-funded research is to determine the involvement of gene imprinting as a mediator of these epigenetic effects. State-of-the-art applied genomic techniques (gene macro-arrays and candidate gene micro-array analyses) will be used to study effects of different nutritional regimens and lactational catabolism, functional nutrients, and inadvertent intra-uterine crowding on early embryonic survival and pre-natal programming in the broader context of comparative animal developmental biology. In the context of an important meat producing species like the pig, the regulation of muscle differentiation (myogenesis) will be a particular focus, as a factor limiting postnatal growth performance.