Talk:Developmental Mechanism - Epithelial Mesenchymal Transition
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Cite this page: Hill, M.A. (2026, October 6) Embryology Developmental Mechanism - Epithelial Mesenchymal Transition. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Developmental_Mechanism_-_Epithelial_Mesenchymal_Transition |
2011
p53 coordinates cranial neural crest cell growth and epithelial-mesenchymal transition/delamination processes
Development. 2011 May;138(9):1827-38. Epub 2011 Mar 29.
Rinon A, Molchadsky A, Nathan E, Yovel G, Rotter V, Sarig R, Tzahor E. Source Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Abstract
Neural crest development involves epithelial-mesenchymal transition (EMT), during which epithelial cells are converted into individual migratory cells. Notably, the same signaling pathways regulate EMT function during both development and tumor metastasis. p53 plays multiple roles in the prevention of tumor development; however, its precise roles during embryogenesis are less clear. We have investigated the role of p53 in early cranial neural crest (CNC) development in chick and mouse embryos. In the mouse, p53 knockout embryos displayed broad craniofacial defects in skeletal, neuronal and muscle tissues. In the chick, p53 is expressed in CNC progenitors and its expression decreases with their delamination from the neural tube. Stabilization of p53 protein using a pharmacological inhibitor of its negative regulator, MDM2, resulted in reduced SNAIL2 (SLUG) and ETS1 expression, fewer migrating CNC cells and in craniofacial defects. By contrast, electroporation of a dominant-negative p53 construct increased PAX7(+) SOX9(+) CNC progenitors and EMT/delamination of CNC from the neural tube, although the migration of these cells to the periphery was impaired. Investigating the underlying molecular mechanisms revealed that p53 coordinates CNC cell growth and EMT/delamination processes by affecting cell cycle gene expression and proliferation at discrete developmental stages; disruption of these processes can lead to craniofacial defects.
PMID 21447558
Evidence for partial epithelial-to-mesenchymal transition (pEMT) and recruitment of motile blastoderm edge cells during avian epiboly
Dev Dyn. 2011 Jun;240(6):1502-11. doi: 10.1002/dvdy.22607. Epub 2011 Mar 15.
Futterman MA, García AJ, Zamir EA. Source Woodruff School of Mechanical Engineering, Parker H. Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, Georgia 30332, USA.
Abstract
Embryonic epiboly has become an important developmental model for studying the mechanisms underlying collective movements of epithelial cells. In the last couple of decades, most studies of epiboly have utilized Xenopus or zebrafish as genetically tractable model organisms, while the avian epiboly model has received virtually no attention. Here, we re-visit epiboly in quail embryos and characterize several molecular markers of epithelial-to-mesenchymal transition (EMT) in the inner zone of the extraembryonic Area Opaca and at the blastoderm edge. Our results show that the intermediate filament vimentin, a widely-used marker for the mesenchymal phenotype, is strongly expressed in the edge cells compared to the cells in the inner zone. Laminin, an extracellular matrix protein that is a major structural and adhesive component of the epiblast basement membrane and the inner zone of the Area Opaca, is notably absent from the blastoderm edge. While these expression profiles are consistent with a mesenchymal phenotype, several other epithelial markers, including cytokeratin, β-catenin, and E-cadherin, are present in the blastoderm edge cells. Moreover, the results of a BrDU proliferation assay strongly suggest that expansion of the edge cell population is primarily due to recruitment of cells from the inner zone, as opposed to proliferation. Taken together, our data show that the edge cells of the avian blastoderm have characteristics of both epithelial and mesenchymal cells, and that the avian epiboly model, which has been dormant for so many years, may yet again prove to be helpful as a unique developmental model for studying partial EMT in the context of collective epithelial cell migration.
Copyright © 2011 Wiley-Liss, Inc.
PMID 21412939
