Oocyte-derived histone H3 lysine 27 methylation controls gene expression in the early embryo


685 demethylase Kdm6b, which removes methyl groups from H3K27. This resulted in loss of H3K27me3 and biallelic expression at the imprinted genes tested6. What could be the role of H3K27me3controlled imprinting? H3K27me3 is regulated by the Polycomb group (PcG) protein Enhancer of Zeste, named EZH2 in mammals. EZH2 ablation in oocytes perturbs embryonic development in the offspring in both mice9 and Drosophila7. Interestingly, in fruit flies, oocyte-acquired H3K27me3 marks many enhancers, which seems to prevent precocious activation of lineage-specific genes at the ‘zygotic genome activation’ (ZGA) stage7. Whether H3K27me3 influences ZGA in mammals is unknown8,10, and the relevance of the H3K27me3-controlled transient imprinting is not yet clear. However, recent studies of the mouse Zdbf2 locus indicate that transient imprinted gene expression before embryo implantation can indeed have profound developmental consequences11. The new mechanism seems particularly important for the trophoblast lineage, in which Epigenetic regulation during gametogenesis and its effects on the next generation have attracted tremendous interest, but the precise mechanisms remain unclear. Imprinted genes are expressed exclusively from the maternal or the paternal allele. DNA methylation is the main regulator of this kind of monoallelic expression in mammals and flowering plants1. Most imprinted mouse loci are controlled by DNA methylation ‘imprints’ that originate from oocyte or sperm2. However, in a previous study, there appeared to be no differential DNA methylation in some imprinted loci3. Furthermore, ablation of the de novo DNA methylation machinery in oocytes did not abolish maternal repression at some imprinted genes in the derived embryos3–5. These and other observations suggest the existence of germline imprints independent of DNA methylation. Recent reports in mice6 and Drosophila7 show that oocyte-acquired patterns of H3K27me3 are transmitted to the zygote and modulate gene expression during early development. The mouse data evoke a novel mode of genomic imprinting that does not require DNA methylation. To screen for imprinted gene loci in mouse zygotes, Azusa Inoue and colleagues mapped DNase-I-hypersensitive sites (DHS)6 and identified hundreds that were present only on the paternal genome. Comparison with recent ChIP-seq data8 revealed that many of these paternal DHS were marked by oocytederived H3K27me3 on the maternal chromosome but showed no differential DNA methylation (Fig. 1). 76 sites showed paternalallele-specific gene expression at the two-cell stage that persisted to the morula stage for 28 genes and to the blastocyst stage for 12 genes. To test the role of maternal H3K27me3, the authors overexpressed in zygotes the Oocyte-derived histone H3 lysine 27 methylation controls gene expression in the early embryo

DOI: 10.1038/nsmb.3456

Cite this paper

@article{Pathak2017OocytederivedHH, title={Oocyte-derived histone H3 lysine 27 methylation controls gene expression in the early embryo}, author={Rakesh Pathak and Robert Feil}, journal={Nature Structural &Molecular Biology}, year={2017}, volume={24}, pages={685-686} }