Open AccessMaternal H3K27me3-dependent autosomal and X chromosome imprinting
Author(s) -
Zhiyuan Chen,
Yi Zhang
Publication year - 2020
Publication title -
nature reviews. genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 26.214
H-Index - 365
eISSN - 1471-0064
pISSN - 1471-0056
DOI - 10.1038/s41576-020-0245-9
Subject(s) - genomic imprinting , imprinting (psychology) , biology , x inactivation , genetics , epigenetics , xist , dna methylation , chromatin , histone , x chromosome , gene , gene expression
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.