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Esrrb Unlocks Silenced Enhancers for Reprogramming to Naive Pluripotency

Adachi, Kenjiro ; Kopp, Wolfgang ; Wu, Guangming ; Heising, Sandra ; Greber, Boris ; Stehling, Martin ; Araúzo-Bravo, Marcos J. ; Boerno, Stefan T. ; Timmermann, Bernd ; Vingron, Martin ; Schöler, Hans R.

Cell stem cell, 2018-08, Vol.23 (2), p.266-275.e6 [Periódico revisado por pares]

United States: Elsevier Inc

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  • Título:
    Esrrb Unlocks Silenced Enhancers for Reprogramming to Naive Pluripotency
  • Autor: Adachi, Kenjiro ; Kopp, Wolfgang ; Wu, Guangming ; Heising, Sandra ; Greber, Boris ; Stehling, Martin ; Araúzo-Bravo, Marcos J. ; Boerno, Stefan T. ; Timmermann, Bernd ; Vingron, Martin ; Schöler, Hans R.
  • Assuntos: DNA methylation ; nucleosome ; pioneer factor ; pluripotency ; reprogramming ; silenced enhancer ; transcription factor
  • É parte de: Cell stem cell, 2018-08, Vol.23 (2), p.266-275.e6
  • Notas: ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
    content type line 23
  • Descrição: Transcription factor (TF)-mediated reprogramming to pluripotency is a slow and inefficient process, because most pluripotency TFs fail to access relevant target sites in a refractory chromatin environment. It is still unclear how TFs actually orchestrate the opening of repressive chromatin during the long latency period of reprogramming. Here, we show that the orphan nuclear receptor Esrrb plays a pioneering role in recruiting the core pluripotency factors Oct4, Sox2, and Nanog to inactive enhancers in closed chromatin during the reprogramming of epiblast stem cells. Esrrb binds to silenced enhancers containing stable nucleosomes and hypermethylated DNA, which are inaccessible to the core factors. Esrrb binding is accompanied by local loss of DNA methylation, LIF-dependent engagement of p300, and nucleosome displacement, leading to the recruitment of core factors within approximately 2 days. These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information. [Display omitted] •Loss of Esrrb leads to incomplete reprogramming of EpiSCs and MEFs to iPSCs•Esrrb can bind to silenced enhancers containing stable nucleosomes and methylated DNA•Esrrb and p300 establish permissive chromatin for core pluripotency TF recruitment•Loss of DNA methylation facilitates LIF-driven nucleosome displacement Rapid reprogramming of epiblast stem cells (EpiSCs) to induced pluripotent stem cells (iPSCs) allows a detailed analysis of epigenetic remodeling induced by transcription factors. The orphan nuclear receptor Esrrb plays a pioneering role in establishing a permissive chromatin environment for the recruitment of core pluripotency factors Oct4, Sox2, and Nanog.
  • Editor: United States: Elsevier Inc
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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