Despite the pivotal role of β-catenin in a variety of biological processes, conditional β-catenin gene ablation in the skin of transgenic mice failed to affect interfollicular epidermal morphogenesis. We elucidated the molecular mechanisms underlying this phenomenon. Long-term cultures of homozygous, heterozygous and β-catenin-null mutant keratinocytes were established to demonstrate that epidermal keratinocyte proliferation, cell cycle progression and cyclin D1 expression occur independently of β-catenin and correlate with repression of transcription from Tcf/Lef-responsive promoters. Moreover, during differentiation,β-catenin-null cells assemble normal intercellular adhesion junctions owing to the substitution of β-catenin with plakoglobin, whereas the expression of the other adhesion components remains unaffected. Taken together, our results demonstrate that epidermal proliferation and adhesion are independent of β-catenin.
β-Catenin is not required for proliferation and differentiation of epidermal mouse keratinocytes
Horst Posthaus, Lina Williamson, Dominique Baumann, Rolf Kemler, Reto Caldelari, Maja M. Suter, Heinz Schwarz, Eliane Müller; β-Catenin is not required for proliferation and differentiation of epidermal mouse keratinocytes. J Cell Sci 1 December 2002; 115 (23): 4587–4595. doi: https://doi.org/10.1242/jcs.00141
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