TGFβ3 signaling activates transcription of the LEF1 gene to induce epithelial mesenchymal transformation during mouse palate development

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TGFβ3 signaling activates transcription of the LEF1 gene to induce epithelial mesenchymal transformation during mouse palate development

Epithelial mesenchymal transformation (EMT) of the medial edge epithelial (MEE) seam creates palatal confluence. This work aims to elucidate the molecular mechanisms by which TGFbeta3 brings about palatal seam EMT. We collected mRNA for PCR analysis from individual transforming MEE cells by laser microdissection techniques and demonstrated that TGFbeta3 stimulates lymphoid-enhancing factor 1 (L...

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Introduction E-cadherin, the primary cell adhesion molecule within adherens junctions, is essential for maintaining apical-basal polarity in epithelial cells (Takeichi, 1988; Hay, 1995). During epithelial-mesenchymal transformation (EMT), loss of E-cadherin expression correlates with a transition to front-end to back-end polarity, leading to subsequent migration of the newly created mesenchymal...

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Epithelial-mesenchymal transformation during craniofacial development.

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IRF6 is the mediator of TGFβ3 during regulation of the epithelial mesenchymal transition and palatal fusion

Mutation in interferon regulatory factor 6 (IRF6) is known to cause syndromic and non-syndromic cleft lip/palate in human. In this study, we investigated the molecular mechanisms related to IRF6 during palatal fusion using palatal shelves organ culture. The results showed that ablation of Irf6 resulted in a delay in TGFβ3-regulated palatal fusion. Ectopic expression of IRF6 was able to promote ...

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TGFbeta3 inhibits E-cadherin gene expression in palate medial-edge epithelial cells through a Smad2-Smad4-LEF1 transcription complex.

Dissociation of medial-edge epithelium (MEE) during palate development is essential for mediating correct craniofacial morphogenesis. This phenomenon is initiated by TGFbeta3 upon adherence of opposing palatal shelves, because loss of E-cadherin causes the MEE seam to break into small epithelial islands. To investigate the molecular mechanisms that cause this E-cadherin loss, we isolated and cu...

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ژورنال

عنوان ژورنال: Journal of Cell Biology

سال: 2003

ISSN: 1540-8140,0021-9525

DOI: 10.1083/jcb.200306024