Genomic imprinting and X-chromosome inactivation (XCI) are classic epigenetic phenomena that involve transcriptional silencing of one parental allele. Germline-derived differential DNA methylation is the best-studied epigenetic mark that initiates imprinting, but evidence indicates that other mechanisms exist. Recent studies have revealed that maternal trimethylation of H3 on lysine 27 (H3K27me3) mediates autosomal maternal allele-specific gene silencing and has an important role in imprinted XCI through repression of maternal Xist. Furthermore, loss of H3K27me3-mediated imprinting contributes to the developmental defects observed in cloned embryos. This novel maternal H3K27me3-mediated non-canonical imprinting mechanism further emphasizes the important role of parental chromatin in development and could provide the basis for improving the efficiency of embryo cloning.

基因组印记和 X 染色体失活 (XCI) 是经典的表观遗传现象，涉及一个亲本等位基因的转录沉默。种系衍生的差异 DNA 甲基化是研究最深入的启动印记的表观遗传标记，但有证据表明存在其他机制。最近的研究表明，赖氨酸 27 (H3K27me3) 上 H3 的母体三甲基化介导常染色体母体等位基因特异性基因沉默，并通过抑制母体Xist在印迹 XCI 中发挥重要作用. 此外，H3K27me3 介导的印记缺失导致在克隆胚胎中观察到的发育缺陷。这种新的母体 H3K27me3 介导的非经典印记机制进一步强调了母体染色质在发育中的重要作用，可以为提高胚胎克隆效率提供基础。