Wnt/Beta-catenin/Esrrb signalling controls the tissue-scale reorganization and maintenance of the pluripotent lineage during murine embryonic diapause

Rui Fan, Yung Su Kim, Jie Wu, Rui Chen, Dagmar Zeuschner, Karina Mildner, Kenjiro Adachi, Guangming Wu, Styliani Galatidou, Jianhua Li, Hans R. Schöler, Sebastian A. Leidel and Ivan Bedzhov ()
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Rui Fan: Max Planck Institute for Molecular Biomedicine
Yung Su Kim: Max Planck Institute for Molecular Biomedicine
Jie Wu: Department of Chemistry and Biochemistry
Rui Chen: Max Planck Institute for Molecular Biomedicine
Dagmar Zeuschner: Max Planck Institute for Molecular Biomedicine
Karina Mildner: Max Planck Institute for Molecular Biomedicine
Kenjiro Adachi: Max Planck Institute for Molecular Biomedicine
Guangming Wu: Max Planck Institute for Molecular Biomedicine
Styliani Galatidou: Max Planck Institute for Molecular Biomedicine
Jianhua Li: Max Planck Institute for Molecular Biomedicine
Hans R. Schöler: Max Planck Institute for Molecular Biomedicine
Sebastian A. Leidel: Department of Chemistry and Biochemistry
Ivan Bedzhov: Max Planck Institute for Molecular Biomedicine

Nature Communications, 2020, vol. 11, issue 1, 1-17

Abstract: Abstract The epiblast, which provides the foundation of the future body, is actively reshaped during early embryogenesis, but the reshaping mechanisms are poorly understood. Here, using a 3D in vitro model of early epiblast development, we identify the canonical Wnt/β-catenin pathway and its central downstream factor Esrrb as the key signalling cascade regulating the tissue-scale organization of the murine pluripotent lineage. Although in vivo the Wnt/β-catenin/Esrrb circuit is dispensable for embryonic development before implantation, autocrine Wnt activity controls the morphogenesis and long-term maintenance of the epiblast when development is put on hold during diapause. During this phase, the progressive changes in the epiblast architecture and Wnt signalling response show that diapause is not a stasis but instead is a dynamic process with underlying mechanisms that can appear redundant during transient embryogenesis.

Date: 2020
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DOI: 10.1038/s41467-020-19353-0

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