ArticleScientific reports2016
Inappropriate cadherin switching in the mouse epiblast compromises proper signaling between the epiblast and the extraembryonic ectoderm during gastrulation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Extracellular presentation of syntaxin4 as a potential trigger for region-specific gastrulation.Cell structure and function · 2025Article
- N2B27 media formulations influence gastruloid development.Development (Cambridge, England) · 2025Article
- Inside-out integrin activation is essential for early mammalian development.Molecular biology of the cell · 2025Article
- BPA Exposure Affects Mouse Gastruloids Axial Elongation by Perturbing the Wnt/β-Catenin Pathway.International journal of molecular sciences · 2024Article
- Defined Microenvironments Trigger In Vitro Gastrulation in Human Pluripotent Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Cadherins in early neural development.Cellular and molecular life sciences : CMLS · 2021Review
- Temporal expression of MOF acetyltransferase primes transcription factor networks for erythroid fate.Science advances · 2020Article
- N-cadherin stabilises neural identity by dampening anti-neural signals.Development (Cambridge, England) · 2019Article
- De novo mutations in MSL3 cause an X-linked syndrome marked by impaired histone H4 lysine 16 acetylation.Nature genetics · 2018Article
- Membrane translocation of t-SNARE protein syntaxin-4 abrogates ground-state pluripotency in mouse embryonic stem cells.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cadherin switching from E-cadherin (E-cad) to N-cadherin (N-cad) is a key step of the epithelial-mesenchymal transition (EMT) processes that occurs during gastrulation and cancer progression. We investigate whether cadherins actively participate in progression of EMT by crosstalk to signaling pathways. We apply ectopic cadherin switching before the onset of mouse gastrulation. Mutants with an induced E-cad to N-cad switch (Ncadki) die around E8.5. Severe morphological changes including a small epiblast, a rounded shape, an enlarged extra-embryonic compartment and lack of the amnion, combined with a massive cell detachment from the ectodermal layer are detected. In contrast to epiblast-specific E-cad depletion, gastrulation is initiated in Ncadki embryos, but patterning of the germ-layers is abnormal. An overall reduction in BMP signaling, expansion of Nodal and Eomes domains, combined with reduced Wnt3a expression at the primitive streak is observed. Our results show that in addition to cadherin-dependent adhesion, proper embryonic development requires E-cad mediated signaling function to facilitate a feedback loop that stabilizes Bmp4 and Bmp2 expression in the extraembryonic ectoderm and sustained downstream activity in the epiblast. Moreover, for proper morphogenesis a fine-tuned spatio-temporal control of cadherin switching is required during EMT at gastrulation to avoid premature cell detachment and migration.
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