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journal.pone.0153591.PDF
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Univ Arizona, Dept Cellular & Mol MedIssue Date
2016-04-20
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Gastrulation EMT Is Independent of P-Cadherin Downregulation 2016, 11 (4):e0153591 PLOS ONEJournal
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© 2016 Moly et al. This is an open access article distributed under the terms of the Creative Commons Attribution License.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Epithelial-mesenchymal transition (EMT) is an evolutionarily conserved process during which cells lose epithelial characteristics and gain a migratory phenotype. Although downregulation of epithelial cadherins by Snail and other transcriptional repressors is generally considered a prerequisite for EMT, recent studies have challenged this view. Here we investigate the relationship between E-cadherin and P-cadherin expression and localization, Snail function and EMT during gastrulation in chicken embryos. Expression analyses show that while E-cadherin transcripts are detected in the epiblast but not in the primitive streak or mesoderm, P-cadherin mRNA and protein are present in the epiblast, primitive and mesoderm. Antibodies that specifically recognize E-cadherin are not presently available. During EMT, P-cadherin relocalizes from the lateral surfaces of epithelial epiblast cells to a circumferential distribution in emerging mesodermal cells. Cells electroporated with an E-cadherin expression construct undergo EMT and migrate into the mesoderm. An examination of Snail function showed that reduction of Slug (SNAI2) protein levels using a morpholino fails to inhibit EMT, and expression of human or chicken Snail in epiblast cells fails to induce EMT. In contrast, cells expressing the Rho inhibitor peptide C3 rapidly exit the epiblast without activating Slug or the mesoderm marker N-cadherin. Together, these experiments show that epiblast cells undergo EMT while retaining P-cadherin, and raise questions about the mechanisms of EMT regulation during avian gastrulation.ISSN
1932-6203Version
Final published versionSponsors
This work was supported by NIH grant P41 HD064559 to PBA.Additional Links
http://dx.plos.org/10.1371/journal.pone.0153591ae974a485f413a2113503eed53cd6c53
10.1371/journal.pone.0153591
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Except where otherwise noted, this item's license is described as © 2016 Moly et al. This is an open access article distributed under the terms of the Creative Commons Attribution License.