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Epigenetics

Across the generations

Nature Reviews Genetics volume 9, pages 248–249 (2008)Cite this article

The histone methylation signature that is observed in the maternal genome depends on the action of the Suv39H histone methyltransferases, which are required for the formation of constitutive heterochromatin and for subsequent gene repression. It was previously observed that, in embryonic stem cells lacking Suv39h1 and Suv39h2 , pericentric heterochromatin acquires trimethylation on lysine 27 of histone H3 (H3K27me3). Peters and colleagues show that, in zygotes, H3K27me3 modifications are enriched at pericentric heterochromatin of paternal origin. This histone modification is typically associated with the Polycomb repressive complexes PRC1 and PRC2. Accordingly, the authors show that components of maternally provided PRC1 accumulate specifically at paternal heterochromatin, although H3K27me3 is not required for PRC1 targeting. The paternal marks are subsequently replaced with maternally associated H3K9me3 by the 16-cell stage, suggesting an initial parental-origin-dependent pathway of heterochromatin formation in the early mouse embryo.

Peters and colleagues further report that, in embryos lacking Suv39h2 from both maternal and zygotic sources, there is also strong enrichment of PRC1 components at maternal heterochromatin. This result suggests that PRC1-dependent histone modification is a default state that is blocked by the presence of Suv39h2-specific marks, and that there is a degree of flexibility in the epigenetic programming that takes place in the early embryo.

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ORIGINAL RESEARCH PAPER

  1. Puschendorf, M. et al. PRC1 and Suv39h specify parental asymmetry at constitutive heterochromatin in early mouse embryos. Nature Genet. 2 Mar 2008 (doi: 10.1038/ng99)

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  1. Senior Editor, Nature Genetics,

    Alan Packer

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  1. Alan Packer
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Packer, A. Across the generations. Nat Rev Genet 9, 248–249 (2008). https://doi.org/10.1038/nrg2357

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  • DOI: https://doi.org/10.1038/nrg2357

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