{beta}-Catenin/LEF1 activated enamelin expression in ameloblast-like cells
- Department of Cariology and Endodontology, Peking University School and Hospital of Stomatology, Beijing 100081 (China)
- Department of Biochemistry and Molecular Biology, Peking University School of Basic Medical Sciences, Beijing 100191 (China)
Research highlights: {yields} {beta}-Catenin/LEF1 complex could activate enamelin gene transcription. {yields} {beta}-Catenin/LEF1 can directly bind to enamelin 5' regulatory region. {yields} Wnt/{beta}-catenin signaling can upregulate enamelin expression in ameloblast-like cells. -- Abstract: Enamelin is an ameloblast-specific matrix protein believed to play essential roles in enamel formation. However, mechanisms of enamelin transcription regulation are not clear. {beta}-Catenin/LEF1 is a key transcriptional complex involved in tooth development. In this study, the role of {beta}-catenin/LEF1 in enamelin expression was investigated. The 5'-flanking region of the mouse enamelin gene was analyzed and cloned. Co-transfection analysis and mutation assays revealed that two conserved LEF1 responsive elements located at -1002 and -597 bp upstream of the enamelin translation initiation site could augment transcriptional activity of the enamelin. The interaction between the enamelin elements and {beta}-catenin/LEF1 was further confirmed by electrophoresis mobility shift assays and chromatin immunoprecipitation assays. In addition, LiCl treatment induced nuclear translocation of {beta}-catenin and elevated endogenous enamelin expression in mouse ameloblast-like cells. The results suggested that Wnt/{beta}-catenin signaling could function in enamelin gene expression by direct interaction through two conserved LEF1 responsive elements on the enamelin gene in ameloblast-like cells.
- OSTI ID:
- 22202717
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 398, Issue 3; Other Information: Copyright (c) 2010 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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