Trim28 is required for epigenetic stability during mouse oocyte to embryo transition.

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Animals, Blastocyst, DNA Methylation, Down-Regulation, Embryo Loss, Embryo, Mammalian, Embryonic Development, Epigenesis, Genetic, Female, Gene Expression Regulation, Developmental, Genomic Imprinting, Insulin-Like Growth Factor II, Male, Mice, Mice, Inbred C57BL, Nuclear Proteins, Oligonucleotide Array Sequence Analysis, Oocytes, Phenotype, RNA, Untranslated, Repressor Proteins

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Science 2012 Mar 23; 335(6075):1499-502.


Phenotypic variability in genetic disease is usually attributed to genetic background variation or environmental influence. Here, we show that deletion of a single gene, Trim28 (Kap1 or Tif1β), from the maternal germ line alone, on an otherwise identical genetic background, results in severe phenotypic and epigenetic variability that leads to embryonic lethality. We identify early and minute epigenetic variations in blastomeres of the preimplantation embryo of these animals, suggesting that the embryonic lethality may result from the misregulation of genomic imprinting in mice lacking maternal Trim28. Our results reveal the long-range effects of a maternal gene deletion on epigenetic memory and illustrate the delicate equilibrium of maternal and zygotic factors during nuclear reprogramming.