Disruptions in epigenetic remodelling during germ cell development may result in the introduction of germline epimutations. These epimutations may cause aberrant gene expression in the developing germline and in the parent’s offspring. This project examines the impacts of depleting polycomb group repressive complex 2 (PRC2) on germline formation and development in the next generation. Preliminary analyses of a mouse model with a point mutation in the epigenetic modifier EED gene, an indispensible component of PRC2, have revealed stochastic variation in somatic and germ cell phenotypes. Homozygous Eed hypomorphic pups exhibit variable survival, with few surviving to adulthood. Immunofluorescent analysis of developing male germ cells in E14.5 embryos revealed variability of molecular markers between different individuals. Fertility tests indicate that males homozygous for the point mutation are subfertile. However, as with the molecular variation observed in E14.5 germ cells and the variable survival of pups, this phenotype is not consistent across all males. As the Eed point mutation results in reduced EED function, rather than complete loss of function, variable penetrance of the mutation may underlie these differences in phenotype. Using whole genome transcriptional profiling we are identifying genes that are consistently misregulated in germ cells due to reduced PRC2 function. This study will provide significant insights into the role of PRC2 in development and epigenetic patterning of the male germline. Greater understanding of epigenetic mechanisms in the developing germline is critical for determining how epigenetic defects in sperm to influence complex inherited diseases in a parent’s children.