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First published online 28 September 2004
doi: 10.1242/jcs.01407

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Mechanical stress induces profound remodelling of keratin filaments and cell junctions in epidermolysis bullosa simplex keratinocytes

¹ Cancer Research UK Cell Structure Research Group, School of Life Sciences, MSI/WTB Complex, University of Dundee, Dundee, DD1 5EH, UK
² Division of Gene Regulation and Expression, School of Life Sciences, MSI/WTB Complex, University of Dundee, Dundee, DD1 5EH, UK
³ Centre for High Resolution Imaging & Processing, School of Life Sciences, MSI/WTB Complex, University of Dundee, Dundee, DD1 5EH, UK

^* Author for correspondence (e-mail: e.b.lane{at}dundee.ac.uk)

Accepted 9 July 2004

The outer epidermal layer of the skin is an epithelium with remarkable protective barrier functions, which is subject to pronounced physical stress in its day-to-day function. A major candidate component for absorbing this stress is the K5/K14 keratin intermediate filament network. To investigate the part played by keratins in stress resilience, keratinocyte cell lines were subjected to mechanical stress. Repeated stretch and relaxation cycles over increasing time produced reproducible changes in the configuration of the keratin network. When wild-type cells were compared with cells carrying a keratin mutation associated with severe epidermolysis bullosa simplex-type skin fragility, the mutant keratin filaments were unable to withstand the mechanical stress and progressively fragmented yielding aggregates and novel ring structures. The cell junctions into which the keratin filaments are normally anchored also progressively disassembled, with all components tested of the cytoplasmic plaques becoming relocated away from the membrane and onto the keratin rings, while integral membrane receptors integrins and cadherins remained at the plasma membrane. The results suggest that maintenance of desmosomes and hemidesmosomes may require some tension, normally mediated by keratin attachments.

Key words: Keratins, Desmosomes, Hemidesmosomes, Stress response, DM-EBS, Keratin mutations

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