Eed, short for Embryonic Ectoderm Development, is a core subunit of the polycomb repressive complex 2 (PRC2). PRC2 is an epigenetic gene silencer responsible for depositing repressive histone H3 lysine 27 trimethylation (H3K27me3) marks on chromatin, leading to gene silencing. Eed functions as a scaffold protein and an H3K27me3-recognizing protein, stabilizing PRC2 and enhancing its activity. Aberrant PRC2 activity, often associated with Eed, is involved in tumorigenesis, making it a potential target for epigenetic cancer therapy [1,2,3,4,7].

In mouse models, loss of microglial Eed impairs synapse density, learning, and memory, suggesting its crucial role in normal synaptic and cognitive functions during postnatal development [5]. Eed deletion from neural stem cells or cerebellar granule cell progenitors in mice leads to reduced proliferation, cell death, cerebellar hypoplasia, and motor deficits, revealing its role in cerebellar development [6]. Conditional knockout of Eed in mice shows its essentiality in regulating the timing of sex-specific primordial germ cell differentiation in both ovaries and testes, as well as X chromosome dosage decompensation in testes [8].

In conclusion, Eed is essential for multiple biological processes including synaptic and cognitive function, cerebellar development, and primordial germ cell differentiation. Its role in cancer, especially through its association with PRC2, makes it an attractive target for therapeutic development. Mouse knockout models have been instrumental in uncovering these functions, providing insights into disease mechanisms and potential treatment strategies for related disorders [1-8].