Abstract
BackgroundDefining how epigenetic information is established in the germline during fetal development is key to understanding how epigenetic information is inherited and impacts on evolution and human health and disease.ResultsHere, we show that Polycomb Repressive Complex 2 is transiently localized in the nucleus of mouse fetal germ cells, while DNA methylation is removed from the germline. This coincides with significant enrichment of trimethylated lysine 27 on histone 3 near the nuclear lamina that is dependent on activity of the essential PRC2 catalytic proteins, Enhancer of Zeste 1 and/or 2.ConclusionsCombined, these data reveal a role for Polycomb Repressive Complex 2 and trimethylated lysine 27 on histone 3 during germline epigenetic programming that we speculate is required to repress target sequences while DNA methylation is removed.
Highlights
Defining how epigenetic information is established in the germline during fetal development is key to understanding how epigenetic information is inherited and impacts on evolution and human health and disease
We identify a key period of transient Polycomb Repressive Complex 2 (PRC2) enrichment in gonadal germ cells as they undergo epigenetic reprogramming
H3K27me3 is highly enriched in fetal germ cells undergoing epigenetic reprogramming Initially, we used quantitative flow cytometric analyses to determine the overall cellular levels of H3K27me3 in E11.5, E13.5 and E15.5 male and female germ cells as they undergo epigenetic reprogramming
Summary
Defining how epigenetic information is established in the germline during fetal development is key to understanding how epigenetic information is inherited and impacts on evolution and human health and disease. To ensure that appropriate epigenetic information is transmitted, germ cells undergo extensive reprogramming during fetal development This allows existing parent-specific information to be reset and potential epigenetic errors to be removed from the germline. The first occurs during proliferation and migration of germ cells in the early embryo and involves reduction of DNA methylation levels from 70 to 30% [1] This is followed by further reductions in DNA methylation as the germ cells enter the developing gonads and initiate sex-specific development. Combining this extensive epigenetic reprogramming results in global DNA methylation levels of ~14 and 7% in male and female germ cells at E13.5, respectively [1]
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