Maternal H3K27me3-dependent autosomal and X chromosome imprinting

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. 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.