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. 2016 May 6;17:94. doi: 10.1186/s13059-016-0952-x

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© Pandolfini et al. 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 8 — Two-layer model of epigenetic control of pluripotency. A marked release from RISC characterizes the ES–ELA transition (priming), whereas transcriptional regulation occurs preferentially at the ELA–NPC transition (neuralization). Our data suggest a causal link between the two phenomena as the pool of de-repressed genes contains distinct chromatin regulators which could overcome the epigenetic barrier between the primed state and ground-state pluripotency. Thus, ground-state miRNAs, which are down-regulated during priming, could shield naïve pluripotent cells from the epigenetic transition required for the onset of embryonic differentiation programs