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

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Bedzhov,  Ivan
Department of Molecular Embryology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Alotaibi,  Hani
Max Planck Society;

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Basilicata,  M. Felicia
Emeritus Group: Molecular Embryology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Ahlborn,  Kerstin
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Stemmler,  Marc P.
Emeritus Group: Molecular Embryology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Bedzhov, I., Alotaibi, H., Basilicata, M. F., Ahlborn, K., Ewa, L., Brabletz, T., et al. (2013). Adhesion, but not a specific cadherin code, is indispensable for ES cell and induced pluripotency. Stem Cell Research, 11, 1250-1263.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002B-8919-6
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.