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It is generally accepted that paternally imprinted X inactivation occurs exclusively in extraembryonic lineages of mouse embryos, whereas cells of the embryo proper, derived from the inner cell mass (ICM), undergo only random X inactivation. Here we show that imprinted X inactivation, in fact, occurs in all cells of early embryos and that the paternal X is then selectively reactivated in cells allocated to the ICM. This contrasts with more differentiated cell types where X inactivation is highly stable and generally irreversible. Our observations illustrate that an important component of genome plasticity in early development is the capacity to reverse heritable gene silencing decisions.

Original publication




Journal article



Publication Date





666 - 669


Acetylation, Animals, Blastocyst, Cell Cycle Proteins, Chromosomal Proteins, Non-Histone, Chromosomes, Mammalian, Dosage Compensation, Genetic, Embryo, Mammalian, Embryonic and Fetal Development, Female, Gene Expression Regulation, Developmental, Genomic Imprinting, Histones, Male, Methylation, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Morula, Polycomb Repressive Complex 2, Proteins, RNA, Long Noncoding, RNA, Untranslated, Repressor Proteins, X Chromosome