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

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      Journal: Nature Structural & Molecular Biology
      Publisher: Springer Nature

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          Abstract

          The monoallelic expression of many imprinted genes in mammals depends on DNA methylation marks that originate from the germ cells. Recent studies in mice and fruit flies evoke a novel, transient mode of genomic imprinting in which oocyte-acquired histone H3 Lys27 trimethylation (H3K27me3) marks are transmitted to the zygote and modulate the allele specificity and timing of gene expression in the early embryo.

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          Maternal H3K27me3 controls DNA methylation-independent genomic imprinting

          Azusa Inoue, Lan Jiang, Lu Falong … (2017)
          Mammalian sperm and oocytes have different epigenetic landscapes and are organized in different fashion. Following fertilization, the initially distinct parental epigenomes become largely equalized with the exception of certain loci including imprinting control regions (ICRs). How parental chromatin becomes equalized and how ICRs escape from this reprogramming is largely unknown. Here we profiled parental allele-specific DNase I hypersensitive sites (DHSs) in mouse zygotes and morula embryos, and investigated the epigenetic mechanisms underlying allelic DHSs. Integrated analyses of DNA methylome and H3K27me3 ChIP-seq data sets revealed 76 genes with paternal allele-specific DHSs that are devoid of DNA methylation but harbor maternal allele-specific H3K27me3. Interestingly, these genes are paternally expressed in preimplantation embryos, and ectopic removal of H3K27me3 induces maternal allele expression. H3K27me3-dependent imprinting is largely lost in the embryonic cell lineage, but at least 5 genes maintain their imprinting in the extra-embryonic cell lineage. The 5 genes include all previously identified DNA methylation-independent imprinted autosomal genes. Thus, our study identifies maternal H3K27me3 as a DNA methylation-independent imprinting mechanism.
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            Chromatin dynamics in the regulation of cell fate allocation during early embryogenesis.

            María N. Padilla, Rachel Burton (2014)
            Following fertilization, gametes undergo epigenetic reprogramming in order to revert to a totipotent state. How embryonic cells subsequently acquire their fate and the role of chromatin dynamics in this process are unknown. Genetic and experimental embryology approaches have identified some of the players and morphological changes that are involved in early mammalian development, but the exact events underlying cell fate allocation in single embryonic cells have remained elusive. Experimental and technological advances have recently provided novel insights into chromatin dynamics and nuclear architecture in single cells; these insights have reshaped our understanding of the mechanisms underlying cell fate allocation and plasticity in early mammalian development.
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              Consequences of the depletion of zygotic and embryonic enhancer of zeste 2 during preimplantation mouse development.

              Andrew J. Bannister, Thomas Jenuwein, Alexander Tarakhovsky … (2003)
              Enhancer of zeste 2 (Ezh2), a SET domain-containing protein, is crucial for development in many model organisms, including early mouse development. In mice, Ezh2 is detected as a maternally inherited protein in the oocyte but its function at the onset of development is unknown. We have used a conditional allele of Ezh2 to deplete the oocyte of this maternal inheritance. We show that the loss of maternal Ezh2 has a long-term effect causing severe growth retardation of neonates despite 'rescue' through embryonic transcription from the paternal allele. This phenotypic effect on growth could be attributed to the asymmetric localisation of the Ezh2/Eed complex and the associated histone methylation pattern to the maternal genome, which is disrupted in Ezh2 mutant zygotes. During subsequent development, we detect distinct histone methylation patterns in the trophectoderm and the pluripotent epiblast. In the latter where Oct4 expression continues from the zygote onwards, the Ezh2/Eed complex apparently establishes a unique epigenetic state and plasticity, which probably explains why loss of Ezh2 is early embryonic lethal and obligatory for the derivation of pluripotent embryonic stem cells. By contrast, in the differentiating trophectoderm cells where Oct4 expression is progressively downregulated Ezh2/Eed complex is recruited transiently to one X chromosome in female embryos at the onset of X-inactivation. This accumulation and the associated histone methylation are also lost in Ezh2 mutants, suggesting a role in X inactivation. Thus, Ezh2 has significant and diverse roles during early development, as well as during the establishment of the first differentiated cells, the trophectoderm, and of the pluripotent epiblast cells.
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                Author and article information

                Journal
                Title: Nature Structural & Molecular Biology
                Abbreviated Title: Nat Struct Mol Biol
                Publisher: Springer Nature
                ISSN (Print): 1545-9993
                ISSN (Electronic): 1545-9985
                Publication date Created: September 7 2017
                Publication date (Print): September 7 2017
                Volume: 24
                Issue: 9
                Pages: 685-686
                Article
                DOI: 10.1038/nsmb.3456
                SO-VID: d61e0459-2c74-4cee-a71d-2f62f8ad9b96
                Copyright © © 2017
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