Environmental influences are thought to alter epigenetic programming in oocytes and contribute to maternally inherited disease. Exposure of the developing germline to particular lifestyle factors can provoke epigenetic alterations in gametes, and thus modify offspring development and phenotype. Embryonic Ectoderm Development (EED) is one of the interdependent subunits of the epigenetic modifier Polycomb Repressive Complex 2 (PRC2), which mediates epigenetic reprogramming in oocytes that is essential for offspring development. PRC2 catalyses the tri-methylation of lysine 27 in histone 3 (H3K27me3) and is enriched in the promotor regions of genes that are developmentally important. Many of these genes play essential roles in stem cell differentiation in fetal and adult tissues, including in developing bone, the hematopoietic system and the brain. The role of PRC2 in epigenetic programming of the egg and sperm and its consequent influence on inherited developmental characteristics and offspring health is currently poorly understood. In humans, de novo germline mutations in EED result in Cohen-Gibson syndrome, which is characterized by fetal overgrowth, accelerated bone aging and skeletal defects. Moreover, we recently established a mouse model in which Eed is specifically deleted in growing oocytes, resulting in eggs that lack EED-dependent epigenetic programming. Heterozygous offspring produced from these eggs were characterised by overgrowth and altered bone density compared to genetically identical heterozygous controls, characteristics reminiscent of Cohen-Gibson syndrome in humans. Embryonic growth plates appear to be altered in offspring from Eed null oocytes as well as trabecular bone composition, indicating accelerated bone development. Using this model, this study aims to determine how EED-dependent programming in oocytes regulates bone development, skeletal phenotype and bone repair in offspring. The outcomes will assist in identifying how inherited epigenetic information controls both early life and long-term developmental outcomes, which is crucial for understanding how epigenetic mechanisms impact the developmental origins of disease.