title: αE-catenin inhibits YAP/TAZ activity to regulate signalling centre formation during tooth development.
abstract: Embryonic signalling centres are specialized clusters of non-proliferating cells that direct the development of many organs. However, the mechanisms that establish these essential structures in mammals are not well understood. Here we report, using the murine incisor as a model, that αE-catenin is essential for inhibiting nuclear YAP localization and cell proliferation. This function of αE-catenin is required for formation of the tooth signalling centre, the enamel knot (EK), which maintains dental mesenchymal condensation and epithelial invagination. EK formation depends primarily on the signalling function of αE-catenin through YAP and its homologue TAZ, as opposed to its adhesive function, and combined deletion of Yap and Taz rescues the EK defects caused by loss of αE-catenin. These findings point to a developmental mechanism by which αE-catenin restricts YAP/TAZ activity to establish a group of non-dividing and specialized cells that constitute a signalling centre.
authors.affiliation: The Research Center and Department of Pathology, Zhongshan Hospital of Dalian University, Dalian 116001, China.|Department of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, California 94143, USA.
authors.forename: Chun-Ying
authors.initials: CY
authors.lastname: Li
authors.affiliation: Department of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, California 94143, USA.
authors.forename: Jimmy
authors.initials: J
authors.lastname: Hu
authors.affiliation: Department of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, California 94143, USA.
authors.forename: Hongbing
authors.initials: H
authors.lastname: Lu
authors.affiliation: Department of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, California 94143, USA.
authors.forename: Jing
authors.initials: J
authors.lastname: Lan
authors.affiliation: Department of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, California 94143, USA.
authors.forename: Wei
authors.initials: W
authors.lastname: Du
authors.affiliation: Department of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, California 94143, USA.
authors.forename: Nicole
authors.initials: N
authors.lastname: Galicia
authors.affiliation: Department of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, California 94143, USA.|Department of Pediatrics and Institute for Human Genetics, University of California, San Francisco, California 94143, USA.
authors.forename: Ophir D
authors.identifier: 0000-0002-6254-7082
authors.initials: OD
authors.lastname: Klein
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics*; D000566:Amelogenesis / Q000235:genetics; D000818:Animals; D018797:Cell Cycle Proteins; D049109:Cell Proliferation / Q000235:genetics; D018507:Gene Expression Regulation, Developmental / Q000235:genetics*; D007180:Incisor / Q000196:embryology*; D051379:Mice; D018345:Mice, Knockout; D009805:Odontogenesis / Q000235:genetics*; D010750:Phosphoproteins / Q000235:genetics*; D014070:Tooth / Q000196:embryology; D015534:Trans-Activators; D000091102:YAP-Signaling Proteins; D051178:alpha Catenin / Q000235:genetics*
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D018797:Cell Cycle Proteins; C495272:Ctnna1 protein, mouse; D010750:Phosphoproteins; D015534:Trans-Activators; C517794:Wwtr1 protein, mouse; D000091102:YAP-Signaling Proteins; C486223:Yap1 protein, mouse; D051178:alpha Catenin