Abstract
Epigenetic regulation is essential for temporal, tissue-specific and parent-of-origin–dependent gene expression. It has recently been found that the mouse Polycomb group (PcG) gene Eed (embryonic ectoderm development) acts to maintain repression of the imprinted X chromosome. Here, we investigated whether Eed is also required for regulation of autosomal imprinted loci. Expression analyses showed that transcripts from the silent alleles of a subset of paternally repressed genes were present in Eed−/− embryos. Parent-of-origin methylation was preserved in these embryos, but we observed changes in the methylation status of specific CpGs in differentially methylated regions (DMRs) at affected but not at unaffected loci. These data identify Eed as a member of a new class of trans-acting factors that regulate parent-of-origin expression at imprinted loci.
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Acknowledgements
We thank D. Threadgill for providing the initial stock of JF1 mice and J. Trasler and T. Bestor for PCR primers and protocols. N.D.M. is supported by a predoctoral fellowship from the Howard Hughes Medical Institute. F.P.-M.V. is the recipient of a Junior Investigator award from the Andrew Mellon Foundation. This work was partially supported by the National Science Foundation to F.P.-M.V. and by the US National Institutes of Health to T.M.
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Mager, J., Montgomery, N., de Villena, FM. et al. Genome imprinting regulated by the mouse Polycomb group protein Eed. Nat Genet 33, 502–507 (2003). https://doi.org/10.1038/ng1125
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DOI: https://doi.org/10.1038/ng1125
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