| Parent of origin effects are unique in that the trait they are associated with is only observed in the offspring if it is inherited from a particular parent, but is not observed if inherited from the other parent. These effects come in several varieties. Within the scope of this dissertation, the effects studied were of three varieties: maternal effects due to oocyte-associated factors, the male Y chromosome, and imprinted genes. Imprinted genes are silenced on one allele in a parent of origin specific manner.; These three sets of parent of origin effects combine to create drastic hybrid effects when two species of deer mice (genus Peromyscus) are mated together. When female P. maniculatus (strain= BW) are crossed to male P. polionotus (strain= PO), the hybrid offspring, though viable and fertile, display significant undergrowth in both embryonic and placental tissues. Conversely, the reciprocal cross (female PO crossed to male BW) yields embryonic lethal overgrowth of both tissues. These effects are at least partially due to reactivation of the normally-silent copy of several imprinted genes.; In this dissertation, we demonstrate genetic evidence that this loss of imprinting phenotype in the large hybrids is due to a maternal effect. Furthermore, we analyze the methylation patterns of imprinted genes, and show that loss of imprinting is associated with a loss of silencing methylation, but only in the placentas of these hybrids. We also show a role for Alkbh1 in placental morphogenesis. We demonstrate that methylated imprint control regions are evolving rapidly under selective pressure. Finally, we show a role for the Y chromosome in uncoupling stress hormone levels and monogamy from glucose metabolism in hybrid males. Taken together these findings provide significant evidence for parent of origin effects as the agents of hybrid dysgenesis in mammals. |
