AI Article Synopsis
- The anterior visceral endoderm (AVE) is crucial for establishing the anterior-posterior axis in mammalian embryos, with its differentiation influenced by signals from the epiblast and gradients from the extraembryonic ectoderm.
- Researchers found that AVE differentiation can still occur in mouse embryonic stem cell aggregates lacking extraembryonic ectoderm, driven by Nodal signaling and possibly regulated by tissue-intrinsic factors.
- β-catenin activity was identified as a key factor that limits AVE formation, suggesting that interactions between the epiblast and visceral endoderm can effectively guide axis patterning in various embryo shapes.
Article 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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11176336 | PMC |
| http://dx.doi.org/10.1038/s41467-024-49380-0 | DOI Listing |
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