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Significance Development of preimplantation embryos entails global DNA demethylation on the zygotic genome. The original thought was that TET-deficient embryos would be unlikely to survive early embryogenesis because they would be unable to mediate genome-wide demethylation in the zygote and preimplantation embryo. However, mice lacking the individual TET proteins Tet1, Tet2, or Tet3 have survived until birth and beyond, suggesting redundancy among TET proteins in the early embryogenesis. Here we report that preimplantation embryos doubly disrupted forTet1 andTet3 show abnormal embryonic phenotypes, whose incomplete penetrance correlates with a high variability of transcriptional profiles and DNA methylation status. Our data suggest that in addition to facilitating DNA demethylation, TET proteins and oxidized methylcytosines may regulate the consistency of gene transcription during embryogenesis.

Simultaneous deletion of the methylcytosine oxidases Tet1 and Tet3 increases transcriptome variability in early embryogenesis