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doi: 10.1242/10.1242/jcs.00141
Research Article |
1 Institute of Animal Pathology, University of Bern, Länggassstr. 122, 3012
Bern, Switzerland
2 Max Planck Institute for Immunobiology, PO Box 1169, Stübeweg 51, 7800
Freiburg Zähringen, Germany
3 Max Planck Institute for Developmental Biology, Spemannstr.35, 72076
Tübingen, Germany
* Author for correspondence (e-mail: eliane.mueller{at}itpa.unibe.ch)
Accepted 4 September 2002
Despite the pivotal role of ß-catenin in a variety of biological processes, conditional ß-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 ß-catenin-null mutant keratinocytes were established to demonstrate that epidermal keratinocyte proliferation, cell cycle progression and cyclin D1 expression occur independently of ß-catenin and correlate with repression of transcription from Tcf/Lef-responsive promoters. Moreover, during differentiation, ß-catenin-null cells assemble normal intercellular adhesion junctions owing to the substitution of ß-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 ß-catenin.
Key words: Keratinocytes, Epidermal renewal, Plakoglobin, Wnt signaling
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