基因组印记
印记(心理学)
生物
X-失活
遗传学
表观遗传学
西斯特
DNA甲基化
染色质
X染色体
组蛋白
基因
基因表达
标识
DOI:10.1038/s41576-020-0245-9
摘要
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. The role of DNA methylation in genomic imprinting and X-chromosome inactivation (XCI) is well documented, but other imprinting mechanisms exist. Here, the authors review the role of oocyte-derived histone H3 lysine 27 trimethylation in establishing autosomal imprinting and imprinted XCI.
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