GSE210397
EED mediates epigenetic repression of developmental genes in growing oocytes and modulates neural and skeletal development in offspring [Bone Samples]
Epigenetic modifications regulate transcriptional access to unique cell-type-specific gene sets, which define cell differentiation and tissue development. Cell-to-cell heritability of this information provides long-term molecular memories that define cell lineage identities. Germline epigenetic programming, including genomic imprinting, can substantially alter offspring development, but the mechanisms are poorly understood. In this study we demonstrate that the essential polycomb complex gene, Eed, regulates histone methylation in a large cohort of non-imprinted developmental genes in mouse and human oocytes. Using a model that facilitates the separation of genetic and epigenetic inheritance, we show that Eed establishes H3K27me3 during a unique widow of early oocyte growth and is essential in mouse oocytes for mediating a complex program that controls fetal growth and co-ordinated development of multiple tissues in late-stage fetal offspring, including bone, brain and placenta. Our study defines a new role for Eed in epigenetic inheritance that profoundly affects offspring growth and development. Overall design: Examination of the impact of EED deletion in oocytes on oocyte epigenetic programming and offspring development