Silencing of β-catenin1 blocks tail regeneration, but does not induce head regeneration in the flatworm Macrostomum lignano
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β-Catenin has two major functions conserved across metazoans. It enables the interaction of classical cadherin with actin at apical junctional complexes and it is the main transcription factor activated by the canonical Wnt pathway. In these two functions, it acts in cell differentiation, proliferation, and in determining the major body axis in early embryos. 4 β-catenin homologs have been described in the highly regenerating planarian flatworm Schmidtea mediterranea . Among them, only Smed-β-catenin1 is involved in establishing posterior identity. Silencing of Smed-β-catenin1 during regeneration leads to head formation in both anterior and posterior wound sites. In regeneration-deficient planarians, β-catenin1 RNAi also rescues head regeneration in posterior pieces. Using phylogenetic inference with β-catenin homologs from a diverse range of flatworms, we found that duplication of β-catenin occurred only in Rhabditophora. In Macrostomum lignano ,there are 3 β-catenin homologs. RNA interference of Mlig-β-catenin1 , but not of Mlig-β-catenin2a or Mlig-β-catenin2b blocked tail regeneration and resulted in the lack of blastema and a strong reduction of cell proliferation at the wound site. After knockdown, tails frequently regenerated imperfectly. At no amputation level could RNAi of any β-catenin rescue head regeneration in M. lignano . These findings demonstrate the requirement for Mlig-β-catenin1 in determining posterior identity and affirms the conserved role of Wnt/β-catenin in specifying the anterior-posterior axis. The failure of head regeneration upon knockdown in M. lignano suggests that the rescue of head regeneration in the absence of β-catenin1 is not a conserved feature in flatworms, but possibly an apomorphy of planarians.