Reinforcement of STAT3 activity reprogrammes human embryonic stem cells to naive-like pluripotency

Hongwei Chen, Irène Aksoy, Fabrice Gonnot, Pierre Osteil, Maxime Aubry, Claire Hamela, Cloé Rognard, Arnaud Hochard, Sophie Voisin, Emeline Fontaine, Magali Mure, Marielle Afanassieff, Elouan Cleroux, Sylvain Guibert, Jiaxuan Chen, Céline Vallot, Hervé Acloque, Clémence Genthon, Cécile Donnadieu, John De Vos, Damien Sanlaville, Jean- François Guérin, Michael Weber, Lawrence W Stanton, Claire Rougeulle, Bertrand Pain, Pierre-Yves Bourillot () and Pierre Savatier ()
Additional contact information
Hongwei Chen: INSERM, U846, Stem Cell and Brain Research Institute
Irène Aksoy: INSERM, U846, Stem Cell and Brain Research Institute
Fabrice Gonnot: INSERM, U846, Stem Cell and Brain Research Institute
Pierre Osteil: INSERM, U846, Stem Cell and Brain Research Institute
Maxime Aubry: INSERM, U846, Stem Cell and Brain Research Institute
Claire Hamela: INSERM, U846, Stem Cell and Brain Research Institute
Cloé Rognard: INSERM, U846, Stem Cell and Brain Research Institute
Arnaud Hochard: INSERM, U846, Stem Cell and Brain Research Institute
Sophie Voisin: INSERM, U846, Stem Cell and Brain Research Institute
Emeline Fontaine: INSERM, U846, Stem Cell and Brain Research Institute
Magali Mure: INSERM, U846, Stem Cell and Brain Research Institute
Marielle Afanassieff: INSERM, U846, Stem Cell and Brain Research Institute
Elouan Cleroux: UMR 7242 Biotechnology and Cell Signaling, University of Strasbourg, CNRS
Sylvain Guibert: UMR 7242 Biotechnology and Cell Signaling, University of Strasbourg, CNRS
Jiaxuan Chen: Stem Cell and Developmental Biology, Genome Institute of Singapore
Céline Vallot: UMR7216 Epigenetics and Cell Fate, CNRS, University of Paris Diderot, Sorbonne Paris Cité
Hervé Acloque: INRA, UMR1388 Génétique, Physiologie et Systèmes d’Elevage
Clémence Genthon: INRA, UMR1388 Génétique, Physiologie et Systèmes d’Elevage
Cécile Donnadieu: INRA, UMR1388 Génétique, Physiologie et Systèmes d’Elevage
John De Vos: INSERM, U1040
Damien Sanlaville: Lyon University Hospital, CNRS UMR 5292, INSERM U1028
Jean- François Guérin: INSERM, U846, Stem Cell and Brain Research Institute
Michael Weber: UMR 7242 Biotechnology and Cell Signaling, University of Strasbourg, CNRS
Lawrence W Stanton: Stem Cell and Developmental Biology, Genome Institute of Singapore
Claire Rougeulle: UMR7216 Epigenetics and Cell Fate, CNRS, University of Paris Diderot, Sorbonne Paris Cité
Bertrand Pain: INSERM, U846, Stem Cell and Brain Research Institute
Pierre-Yves Bourillot: INSERM, U846, Stem Cell and Brain Research Institute
Pierre Savatier: INSERM, U846, Stem Cell and Brain Research Institute

Nature Communications, 2015, vol. 6, issue 1, 1-17

Abstract: Abstract Leukemia inhibitory factor (LIF)/STAT3 signalling is a hallmark of naive pluripotency in rodent pluripotent stem cells (PSCs), whereas fibroblast growth factor (FGF)-2 and activin/nodal signalling is required to sustain self-renewal of human PSCs in a condition referred to as the primed state. It is unknown why LIF/STAT3 signalling alone fails to sustain pluripotency in human PSCs. Here we show that the forced expression of the hormone-dependent STAT3-ER (ER, ligand-binding domain of the human oestrogen receptor) in combination with 2i/LIF and tamoxifen allows human PSCs to escape from the primed state and enter a state characterized by the activation of STAT3 target genes and long-term self-renewal in FGF2- and feeder-free conditions. These cells acquire growth properties, a gene expression profile and an epigenetic landscape closer to those described in mouse naive PSCs. Together, these results show that temporarily increasing STAT3 activity is sufficient to reprogramme human PSCs to naive-like pluripotent cells.

Date: 2015
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DOI: 10.1038/ncomms8095

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