Regensburg 2013 – wissenschaftliches Programm
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BP: Fachverband Biologische Physik
BP 24: Posters: Physics of Cells
BP 24.21: Poster
Mittwoch, 13. März 2013, 17:30–19:30, Poster C
Plectin contributes to the mechanical stability of keratinocytes and myoblasts — •Navid Bonakdar1, Achim Schilling1, Pablo Lennert1, Michael Kuhn1, Astrid Mainka1, Wolfgang Goldmann1, Gerhard Wiche2, and Ben Fabry1 — 1Biophysics, University of Erlangen-Nuremberg, Germany — 2Biochemistry and Cell Biology, University of Vienna, Austria
Plectin and its isoforms are promiscuous crosslinkers of actin filaments, microtubules and intermediate filaments (IF) in a wide variety of cell types. In epithelial cells and keratinocytes, it is also found in hemidesmosomes that link the laminin receptor a6b4 with the keratin IFs. Mutations in the plectin gene cause a skin blistering disorder (epidermolysis bullosa) that is also associated with a late-onset of muscular dystrophy. In both disorders, mechanical alterations of the keratinocytes and the myoblasts, respectively, are thought to be ultimately responsible for the pathological manifestation. To test this hypothesis, we measured the mechanical properties of plectin knockout and plectin-expressing mouse keratinocytes and myoblasts with a high force magnetic tweezer device. We found that in plectin-deficient myoblasts, stiffness, tractions, and adhesive strength were about 2-fold reduced, indicating that plectin is important for the mechanical stability of these cells. In contrast, plectin-deficient keratinocytes assessed under similar conditions were found to show other effects. Our results demonstrate that human diseases associated with plectin mutations have a cell mechanical origin, and that plectin affects the cytoskeleton in different cell types in distinct ways.