Beta-Catenin Is Vital for the Integrity of Mouse Embryonic Stem Cells

beta-catenin mediated Wnt-signaling is assumed to play a major function in embryonic stem cells in maintaining their stem cell character and the exit from this unique trait. The complexity of beta-catenin action and conflicting results on the role of beta-catenin in maintaining the pluripotent state have made it difficult to understand its precise cellular and molecular functions. To attempt this issue we have generated new genetically modified mouse embryonic stem cell lines allowing for the deletion of beta-catenin in a controlled manner by taking advantage of the Cre-ER-T2 system and analyzed the effects in a narrow time window shortly after ablation. By using this approach, rather then taking long term cultured beta-catenin null cell lines we demonstrate that beta-catenin is dispensable for the maintenance of pluripotency associated genes. In addition we observed that the removal of beta-catenin leads to a strong increase of cell death, the appearance of multiple clustered functional centrosomes most likely due to a mis-regulation of the polo-like-kinase 2 and furthermore, alterations in chromosome segregation. Our study demonstrates the importance of beta-catenin in maintaining correct cellular functions and helps to understand its role in embryonic stem cells.