Journal
NATURE
Volume 484, Issue 7394, Pages 339-U74Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature10960
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Funding
- NIH [5DP1OD003958, 5RC1AA019317, U01ES017155, P01GM099117]
- HHMI
- Harvard Stem Cell Institute
- Massachusetts Life Science Center
- Pew Charitable Trusts
- Center for Excellence in Genome Science from the NHGRI [1P50HG006193-01]
- Burroughs Wellcome Career Award at the Scientific Interface
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DNA methylation is highly dynamic during mammalian embryogenesis. It is broadly accepted that the paternal genome is actively depleted of 5-methylcytosine at fertilization, followed by passive loss that reaches a minimum at the blastocyst stage. However, this model is based on limited data, and so far no base-resolution maps exist to support and refine it. Here we generate genome-scale DNA methylation maps in mouse gametes and from the zygote through post-implantation. We find that the oocyte already exhibits global hypomethylation, particularly at specific families of long interspersed element 1 and long terminal repeat retroelements, which are disparately methylated between gametes and have lower methylation values in the zygote than in sperm. Surprisingly, the oocyte contributes a unique set of differentially methylated regions (DMRs)-including many CpG island promoters-that are maintained in the early embryo but are lost upon specification and absent from somatic cells. In contrast, sperm-contributed DMRs are largely intergenic and become hypermethylated after the blastocyst stage. Our data provide a genome-scale, base-resolution timeline of DNA methylation in the pre-specified embryo, when this epigenetic modification is most dynamic, before returning to the canonical somatic pattern.
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