1. A C-terminally truncated form of β-catenin acts as a novel regulator of Wnt/β-catenin signaling in planarians.
- Author
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Su H, Sureda-Gomez M, Rabaneda-Lombarte N, Gelabert M, Xie J, Wu W, and Adell T
- Subjects
- Animals, Armadillo Domain Proteins genetics, Armadillo Domain Proteins metabolism, Evolution, Molecular, Homeostasis, Models, Biological, Peptide Fragments antagonists & inhibitors, Peptide Fragments genetics, Peptide Fragments metabolism, Photoreceptor Cells, Invertebrate physiology, Planarians genetics, Planarians growth & development, Protein Interaction Domains and Motifs, Regeneration, TCF Transcription Factors genetics, TCF Transcription Factors metabolism, beta Catenin antagonists & inhibitors, beta Catenin genetics, gamma Catenin genetics, gamma Catenin metabolism, Planarians physiology, Wnt Signaling Pathway, beta Catenin metabolism
- Abstract
β-Catenin, the core element of the Wnt/β-catenin pathway, is a multifunctional and evolutionarily conserved protein which performs essential roles in a variety of developmental and homeostatic processes. Despite its crucial roles, the mechanisms that control its context-specific functions in time and space remain largely unknown. The Wnt/β-catenin pathway has been extensively studied in planarians, flatworms with the ability to regenerate and remodel the whole body, providing a 'whole animal' developmental framework to approach this question. Here we identify a C-terminally truncated β-catenin (β-catenin4), generated by gene duplication, that is required for planarian photoreceptor cell specification. Our results indicate that the role of β-catenin4 is to modulate the activity of β-catenin1, the planarian β-catenin involved in Wnt signal transduction in the nucleus, mediated by the transcription factor TCF-2. This inhibitory form of β-catenin, expressed in specific cell types, would provide a novel mechanism to modulate nuclear β-catenin signaling levels. Genomic searches and in vitro analysis suggest that the existence of a C-terminally truncated form of β-catenin could be an evolutionarily conserved mechanism to achieve a fine-tuned regulation of Wnt/β-catenin signaling in specific cellular contexts.
- Published
- 2017
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