Augmented BMP signaling commits cranial neural crest cells to a chondrogenic fate by suppressing autophagic β-catenin degradation
Jingwen Yang, Megumi Kitami, Haichun Pan, Masako Toda Nakamura, Honghao Zhang, Fei Liu, Lingxin Zhu, Yoshihiro Komatsu, Yuji Mishina
Abstract
mutants. Our results suggest that BMP signaling and autophagy coordinately regulate β-catenin activity to direct the fate of CNCCs during craniofacial development. These findings may also explain why some patients with FOP develop ectopic bones through endochondral ossification in craniofacial regions.
Topics & Concepts
Cell biologyAutophagyChondrogenesisNeural crestDegradation (telecommunications)CateninChemistryWnt signaling pathwayBone morphogenetic protein 2Beta-cateninSignal transductionMesenchymal stem cellBiologyBiochemistryComputer scienceApoptosisEmbryoIn vitroTelecommunicationsCancer-related gene regulationCancer-related molecular mechanisms researchHedgehog Signaling Pathway Studies