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Nat Cell Biol. 2016 Nov;18(11):1139-1148. doi: 10.1038/ncb3418. Epub 2016 Oct 10.

Mitotic binding of Esrrb marks key regulatory regions of the pluripotency network.

Author information

1
Epigenetics of Stem Cells, Department of Developmental &Stem Cell Biology, Institut Pasteur, CNRS UMR 3738, 25 rue du docteur Roux, 75015 Paris, France.
2
Mouse Functional Genetics, Department of Developmental &Stem Cell Biology, Institut Pasteur, CNRS UMR 3738, 25 rue du docteur Roux, 75015 Paris, France.
3
Imaging and Modelling, Department of Cell Biology &Infections, Institut Pasteur, CNRS UMR 3691, 25 rue du docteur Roux, Paris 75015, France.
4
Transcriptome and EpiGenome, BioMics, Center for Innovation and Technological Research, Institut Pasteur, 28 rue du docteur Roux, 75015 Paris, France.

Abstract

Pluripotent mouse embryonic stem cells maintain their identity throughout virtually infinite cell divisions. This phenomenon, referred to as self-renewal, depends on a network of sequence-specific transcription factors (TFs) and requires daughter cells to accurately reproduce the gene expression pattern of the mother. However, dramatic chromosomal changes take place in mitosis, generally leading to the eviction of TFs from chromatin. Here, we report that Esrrb, a major pluripotency TF, remains bound to key regulatory regions during mitosis. We show that mitotic Esrrb binding is highly dynamic, driven by specific recognition of its DNA-binding motif and is associated with early transcriptional activation of target genes after completion of mitosis. These results indicate that Esrrb may act as a mitotic bookmarking factor, opening another perspective to molecularly understand the role of sequence-specific TFs in the epigenetic control of self-renewal, pluripotency and genome reprogramming.

PMID:
27723719
DOI:
10.1038/ncb3418
[Indexed for MEDLINE]

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