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Epithelial cell plasticity drives endoderm formation during gastrulation.

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Mesoderm forms via epithelial-to-mesenchymal transition (EMT), while endoderm development avoids EMT. Forkhead box transcription factor A2 (Foxa2) maintains endoderm

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Area of Science:

  • Developmental Biology
  • Cell Biology
  • Genetics

Background:

  • Epiblast cells ingress into the primitive streak via epithelial-to-mesenchymal transition (EMT) to form mesoderm.
  • Mechanisms governing endoderm acquisition of epithelial fate remain less understood.

Purpose of the Study:

  • To resolve morphogenetic programs segregating mesoderm and endoderm germ layers.
  • To elucidate the mechanisms of endoderm epithelial fate acquisition.

Main Methods:

  • Utilized embryonic stem cell and mouse embryo knock-in reporter systems.
  • Combined time-resolved lineage labeling with high-resolution single-cell transcriptomics.

Main Results:

  • Mesoderm formation occurs through classical EMT.
  • Endoderm formation is independent of the EMT transcription factor Snail1, involving epithelial cell plasticity.
  • Forkhead box transcription factor A2 (Foxa2) acts as an epithelial gatekeeper, suppressing EMT in endoderm.

Conclusions:

  • Established detailed morphogenetic programs for germ layer formation (mesoderm and endoderm).
  • Demonstrated distinct mechanisms for mesoderm and endoderm development.
  • Highlighted the role of Foxa2 in maintaining endoderm epithelial fate.
  • Findings have implications for stem cell differentiation and understanding cancer metastasis.