5-Hydroxymethylcytosine in the mammalian zygote is linked with epigenetic reprogramming

Mark Wossidlo, Toshinobu Nakamura, Konstantin Lepikhov, C. Joana Marques, Valeri Zakhartchenko, Michele Boiani, Julia Arand, Toru Nakano, Wolf Reik and Jörn Walter ()
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Mark Wossidlo: Saarland University
Toshinobu Nakamura: Medical School and Graduate School of Frontier Biosciences, Osaka University
Konstantin Lepikhov: Saarland University
C. Joana Marques: Laboratory of Developmental Genetics and Imprinting, The Babraham Institute
Valeri Zakhartchenko: Ludwig-Maximilian University
Michele Boiani: Max-Planck-Institut für molekulare Biomedizin
Julia Arand: Saarland University
Toru Nakano: Medical School and Graduate School of Frontier Biosciences, Osaka University
Wolf Reik: Laboratory of Developmental Genetics and Imprinting, The Babraham Institute
Jörn Walter: Saarland University

Nature Communications, 2011, vol. 2, issue 1, 1-8

Abstract: Abstract The epigenomes of early mammalian embryos are extensively reprogrammed to acquire a totipotent developmental potential. A major initial event in this reprogramming is the active loss/demethylation of 5-methylcytosine (5mC) in the zygote. Here, we report on findings that link this active demethylation to molecular mechanisms. We detect 5-hydroxymethylcytosine (5hmC) as a novel modification in mouse, bovine and rabbit zygotes. On zygotic development 5hmC accumulates in the paternal pronucleus along with a reduction of 5mC. A knockdown of the 5hmC generating dioxygenase Tet3 simultaneously affects the patterns of 5hmC and 5mC in the paternal pronucleus. This finding links the loss of 5mC to its conversion into 5hmC. The maternal pronucleus seems to be largely protected against this mechanism by PGC7/Dppa3/Stella, as in PGC7 knockout zygotes 5mC also becomes accessible to oxidation into 5hmC. In summary, our data suggest an important role of 5hmC and Tet3 for DNA methylation reprogramming processes in the mammalian zygote.

Date: 2011
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DOI: 10.1038/ncomms1240

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