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Homeodomain-Mediated β-Catenin-Dependent Switching Events Dictate Cell-Lineage Determination

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Kemler,  Rolf
Emeritus Group: Molecular Embryology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Grosschedl,  Rudolf
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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引用

Olson, L. E., Tollkuhn, J., Scafoglio, C., Krones, A., Zhang, J., Ohgi, K. A., Wu, W., Taketo, M., Kemler, R., Grosschedl, R., Rose, D., & Li, X. (2006). Homeodomain-Mediated β-Catenin-Dependent Switching Events Dictate Cell-Lineage Determination. Cell, 125, 593-605. doi:10.1016/j.cell.2006.02.046.


引用: https://hdl.handle.net/11858/00-001M-0000-002B-9254-A
要旨
While the biological roles of canonical Wnt/β-catenin signaling in development and disease are well documented, understanding the molecular logic underlying the functionally distinct nuclear transcriptional programs mediating the diverse functions of β-catenin remains a major challenge. Here, we report an unexpected strategy for β-catenin-dependent regulation of cell-lineage determination based on interactions between β-catenin and a specific homeodomain factor, Prop1, rather than Lef/Tcfs. β-catenin acts as a binary switch to simultaneously activate expression of the critical lineage-determining transcription factor, Pit1, and to repress the gene encoding the lineage-inhibiting transcription factor, Hesx1, acting via TLE/Reptin/HDAC1 coreprossor complexes. The strategy of functionally distinct actions of a homeodomain factor in response to Wnt signaling is suggested to be prototypic of a widely used mechanism for generating diverse cell types from pluripotent precursor cells in response to common signaling pathways during organogenesis.