Pramel7 mediates ground-state pluripotency through proteasomal-epigenetic combined pathways

Graf, Urs; Casanova, Elisa A; Wyck, Sarah; Dalcher, Damian; Gatti, Marco; Vollenweider, Eva; Okoniewski, Michal J; Weber, Fabienne A; Patel, Sameera S; Schmid, Marc W; Li, Jiwen; Sharif, Jafar; Wanner, Guido A; Koseki, Haruhiko; Wong, Jiemin; Pelczar, Pawel; Penengo, Lorenza; Santoro, Raffaella; Cinelli, Paolo

doi:10.1038/ncb3554

Citations

Citation copied

Graf, U., Casanova, E. A., Wyck, S., Dalcher, D., Gatti, M., Vollenweider, E., Okoniewski, M. J., Weber, F. A., Patel, S. S., Schmid, M. W., Li, J., Sharif, J., Wanner, G. A., Koseki, H., Wong, J., Pelczar, P., Penengo, L., Santoro, R., & Cinelli, P. (2017). Pramel7 mediates ground-state pluripotency through proteasomal-epigenetic combined pathways. Nature Cell Biology, 19(7), 763–773. https://doi.org/10.1038/ncb3554

Abstract

Naive pluripotency is established in preimplantation epiblast. Embryonic stem cells (ESCs) represent the immortalization of naive pluripotency. 2i culture has optimized this state, leading to a gene signature and DNA hypomethylation closely comparable to preimplantation epiblast, the developmental ground state. Here we show that Pramel7 (PRAME-like 7), a protein highly expressed in the inner cell mass (ICM) but expressed at low levels in ESCs, targets for proteasomal degradation UHRF1, a key factor for DNA methylation maintenance. Inc