Epigenetic regulation of embryonic ectoderm development in stem cell differentiation and transformation during ontogenesis

Dynamic chromatin accessibility regulates stem cell fate determination and tissue homeostasis via controlling gene expression. As a histone-modifying enzyme that predominantly mediates methylation of lysine 27 in histone H3 (H3K27me1/2/3), Polycomb repressive complex 2 (PRC2) plays the canonical role in targeting developmental regulators during stem cell differentiation and transformation. Embryonic ectoderm development (EED), the core scaffold subunit of PRC2 and as an H3K27me3-recognizing protein, has been broadly implicated with PRC2 stabilization and allosterically stimulated PRC2. Accumulating evidences from experimental data indicate that EED-associating epigenetic modifications are indispensable for stem cell maintenance and differentiation into specific cell lineages. In this review, we discuss the most updated advances to summarize the structural architecture of EED and its contributions and underlying mechanisms to mediating lineage differentiation of different stem cells during epigenetic modification to expand our understanding of PRC2.

Automated summary

Dynamic chromatin accessibility controls gene expression, regulating stem cell fate determination and tissue homeostasis. Polycomb repressive complex 2 (PRC2), as a histone-modifying enzyme that predominantly mediates methylation of lysine 27 in histone H3 (H3K27me1/2/3), plays a canonical role in targeting developmental regulators during stem cell differentiation. Embryonic ectoderm development (EED), the core scaffold subunit of PRC2 and an H3K27me3-recognizing protein, is involved in PRC2 stabilization and allosterically stimulated PRC2. Experimental data suggest that EED-associated epigenetic modifications are essential for stem cell maintenance and differentiation. This review discusses the structural architecture of EED, its contributions, and underlying mechanisms in mediating lineage differentiation of different stem cells during epigenetic modification to enhance our understanding of PRC2.