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 Available to Purchase
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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