Trim28 Is Required for Epigenetic Stability During Mouse Oocyte to Embryo Transition

Author:

Messerschmidt Daniel M.1,de Vries Wilhelmine2,Ito Mitsuteru3,Solter Davor14,Ferguson-Smith Anne35,Knowles Barbara B.16

Affiliation:

1. Mammalian Development Group, Institute of Medical Biology, 138648 Singapore.

2. The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA.

3. Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK.

4. Duke-NUS, Graduate Medical School, 169857 Singapore.

5. Singapore Institute for Clinical Sciences, 117609 Singapore.

6. Department of Biochemistry, National University of Singapore, 117597 Singapore.

Abstract

Trimprinting the Genome Reprogramming the parental genomes during the oocyte-to-embryo transition requires highly controlled epigenetic mechanisms. Although resetting the genome to a ground state is essential, conservation of inheritable marks is equally important. Now, Messerschmidt et al. (p. 1499 ) demonstrate that maternal deletion of the epigenetic modifier Trim28 in mice results in a strongly variable, yet ultimately embryonic, lethal phenotype. Aberrant loss of DNA methylation at imprinting control regions and thus partial loss of epigenetic memory was responsible for the phenotype. The stochastic time and mode of embryonic death reflect the exquisitely balanced interplay of maternal and zygotic factors in the early mammalian embryo.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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