Ezh1, the enhancer of zeste homolog 1, is an epigenetic silencing factor. As a core component of polycomb repressive complex 2 (PRC2), it mediates the mono-, di-and tri-methylation of histone H3 lysine 27 (H3K27me1/2/3), playing key roles in cell growth and differentiation [1,3]. It is involved in multiple biological processes such as embryonic hematopoiesis, oocyte meiosis, and neurogenesis [2,5,6].

In iPSC-derived T cell differentiation, Ezh1 repression facilitates in vitro differentiation and maturation of T cells, generating cells with enhanced antitumor activity [2]. In mouse oocytes and early embryos, maternal Ezh1/2 deficiency impairs mitochondrial structure and function, leading to oxidative stress, autophagy interference, and apoptosis [4]. In oocyte meiosis prophase I in mice, Ezh1/2 is essential for oocyte development, and its deficiency causes failure of DNA double-strand breaks repair and meiotic progression arrest [5]. In neurogenesis, both gain-and loss-of-function variants in Ezh1 disrupt neural progenitor cell differentiation, causing neurodevelopmental disorders [6].

In conclusion, Ezh1 is crucial for various biological processes including cell differentiation, oocyte and embryo development, and neurogenesis. Studies using gene knockout models in mice have revealed its role in these processes and associated disease conditions such as impaired T cell-based cancer immunotherapy, abnormal oocyte and embryo development, and neurodevelopmental disorders.