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- Title
Tissue-intrinsic beta-catenin signals antagonize Nodal-driven anterior visceral endoderm differentiation.
- Authors
Schumacher, Sina; Fernkorn, Max; Marten, Michelle; Chen, Rui; Kim, Yung Su; Bedzhov, Ivan; Schröter, Christian
- Abstract
The anterior-posterior axis of the mammalian embryo is laid down by the anterior visceral endoderm (AVE), an extraembryonic signaling center that is specified within the visceral endoderm. Current models posit that AVE differentiation is promoted globally by epiblast-derived Nodal signals, and spatially restricted by a BMP gradient established by the extraembryonic ectoderm. Here, we report spatially restricted AVE differentiation in bilayered embryo-like aggregates made from mouse embryonic stem cells that lack an extraembryonic ectoderm. Notably, clusters of AVE cells also form in pure visceral endoderm cultures upon activation of Nodal signaling, indicating that tissue-intrinsic factors can restrict AVE differentiation. We identify β-catenin activity as a tissue-intrinsic factor that antagonizes AVE-inducing Nodal signals. Together, our results show how an AVE-like population can arise through interactions between epiblast and visceral endoderm alone. This mechanism may be a flexible solution for axis patterning in a wide range of embryo geometries, and provide robustness to axis patterning when coupled with signal gradients. The anterior visceral endoderm is an important cell population that positions the head-to-tail axis of the mammalian embryo. Here, Schumacher et al. identify beta-catenin signaling as a key regulator of anterior visceral endoderm differentiation.
- Subjects
ENDODERM; EMBRYONIC stem cells; MAMMALIAN embryos; WNT signal transduction; CELL populations; ECTODERM
- Publication
Nature Communications, 2024, Vol 15, Issue 1, p1
- ISSN
2041-1723
- Publication type
Article
- DOI
10.1038/s41467-024-49380-0