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  • Previous evidence suggests that PRC is an

    2022-08-04

    Previous evidence suggests that PRC2 is an important regulator of chromatin looping interactions in embryonic stem clobetasol price synthesis . The new study by Donaldson-Collier and colleagues provides the first evidence that similar processes may be at play in lymphoma. It is still largely unclear, however, both in normal and disease contexts, how PRC2 activity is functionally linked to chromatin looping. It is tempting to speculate that the changes in H3K27me3 deposition and chromatin looping are functionally linked through the binding of canonical PRC1. In support, CBX8-containing canonical PRC1 complexes were recently shown to be essential to maintain the repression of genes silenced by mutant EZH2 activity in lymphoma .
    Introduction The development of early-stage mammal embryos is accompanied by changes in epigenetic modifications, such as DNA methylation, histone modifications, and X chromosome inactivation [1]. Since these changes occur rapidly during the first few cell divisions before the onset of transcription, factors stored in the oocyte (e.g. mRNA and proteins) are likely to induce them [2]. However, the function of many maternal epigenetic modifiers in early embryonic development remains unclear. Enhancer of zeste 2 (EZH2) is known as the catalytic subunit of Polycomb Repressive Complex 2 (PRC2) and functions as a histone–lysine N-methyltransferase of H3K27me3. The other two subunits of PRC2 are suppressor of zeste 12 homologue (SUZ12) and embryonic ectoderm development (EED) [3,4]. SUZ12 ensures the stability of EZH2 and facilitates nucleosome recognition [5,6], while EED is required to link EZH2 to histone H3 [7]. EZH2 interacts with EED via its domain II, which is conserved between Drosophila and mammals [8]. There is evidence in mice and human ES cells that PRC2 is able to repress various markers of cell differentiation [9,10], suggesting that PCR2 is implicated in regulating ESC differentiation. Especially, EZH2 has been shown to be critical for mouse ESC differentiation, as ESCs lacking Ezh2 show aberrant expression patterns of key differentiation regulators [11]. Together, these findings suggest that EZH2 is involved in regulating early embryogenesis and maintaining ESC identity, which is consistent with the observation that EZH2 is expressed during early embryonic development and in ESCs. EZH2 may achieve these roles by methylating H3K27 and regulating its target genes. Interestingly, there is research suggesting that the roles of EZH2 in histone methylation and maintenance of ESC identity can be partially complemented by EZH1, a homologue of EZH2. Unlike EZH2, EZH1 is preferentially expressed in differentiated adult tissues [12,13]. It has been shown in ESCs that EZH1 plays a role in determining the levels of H3K27me3 at a subset of PRC2 regulated genes. Depletion of Ezh1 in cells lacking Ezh2 resulted in the abolishment of residual methylation on H3K27 and the derepression of H3K27me3 target genes [11,14], suggesting that Ezh1 may help to ensure the effect of EZH2 on H3K27 methylation. However, EZH2 may also have independent functions that do not involve H3K27 methylation [15,16]. A recent study reported that the Ezh2 could directly regulate the epigenetic status of the NANOG promoter, suggesting a role for Ezh2 in regulating NANOG expression. This is consistent with the observation that the loss of Ezh2 in iPS cells is accompanied by increased levels of Nanog [17]. On the other hand, it has also been reported that Ezh2 can be negatively regulated in mouse preimplantation embryos by Oct4 and Sox2 at the post-translational level [18]. Since Oct4, Nanog and Sox2 are required for maintaining pluripotency in ESCs, these results suggest that EZH2 is critical to ensure the equilibrium between ESC self-renewal and differentiation. Given that the dynamics of early embryonic development also involves control of pluripotency and differentiation, which are primarily regulated by the maternal genome. However, little is known about the effect of maternal EZH2 on porcine early embryonic development. Considering the potential confounding influence of polyspermy, we aimed to investigate the expression patterns of EZH2 and its function during porcine preimplantation development using parthenogenetic embryos.