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      Adhesion, but not a specific cadherin code, is indispensable for ES cell and induced pluripotency.

      Stem Cell Research
      Animals, Cadherins, deficiency, genetics, metabolism, Cell Adhesion, Cell Differentiation, Cells, Cultured, Embryonic Stem Cells, cytology, Epithelial-Mesenchymal Transition, Gene Knock-In Techniques, Genetic Loci, Homeodomain Proteins, Induced Pluripotent Stem Cells, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Nude, Recombinant Fusion Proteins

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          Abstract

          Embryonic stem (ES) cell pluripotency and induced pluripotent stem (iPS) cell generation is dependent on a core transcriptional network and proper cell-cell adhesion mediated by E-cadherin (E-cad). Whereas E-cad is associated with pluripotency, N-cadherin (N-cad) expression is correlated with differentiation into mesodermal and neuroectodermal lineages. We investigated whether E-cad harbors unique molecular features in establishing or maintaining pluripotency. By using a gene replacement knock-in (ki) approach to express N-cadherin (N-cad) or E-cad/N-cad chimeric cadherins under the control of the E-cad locus, we show that all E-cad-depleted ki/ki ES cells are maintained in an undifferentiated state. Surprisingly, these cells retained key features of pluripotency, such as Nanog expression and full differentiation capacity in vitro and in vivo, whereas E-cad knockout (ko) ES cells irreversibly lost most of these features. Moreover, our results indicate that E-cad mediated adhesion is essential for iPS cell generation, since E-cad depleted fibroblasts were not reprogrammed. In contrast, N-cad efficiently supports somatic reprogramming similar to E-cad, and permits initiation of the crucial initial step of mesenchymal-epithelial transition. Thus, we show that cell adhesion and a robust pluripotent phenotype are ultimately connected. Since N-cad properly compensates for loss of E-cad, no specific 'cadherin code' is required. © 2013.

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