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THE COUPLING OF VINCULIN TO THE CYTOSKELETON IS NOT ESSENTIAL FOR MECHANO‐CHEMICAL SIGNALING IN F9 CELLS

It is well established that mechanical forces can regulate cell growth and guide tissue remodeling, yet little is known about how mechanical signals act at the cell surface membrane to produce biochemical changes in the cell. To explore this question, I used a mouse embryonic F9 vinculin‐deficient cell line (γ229), which, unlike wild‐type cells, shows no fibronectin‐dependent cell spreading. The wild‐type cell line exhibited a twofold increase in area over four hours. I observed (i) an earlier rise in intracellular free calcium from ∼0.2 to ∼3μm in wild‐type compared with γ229 cells, thus similar calcium levels after 4h; (ii) an initial higher ratio of p‐MAP/MAP‐Kinase for γ229, but similar FA‐Kinase activation; and (iii) a marginal change in intracellular pH [pH]i in both F9 cell lines. When I applied controlled local stresses directly to integrin receptors using RGD‐coated magnetic beads, they displaced to a lesser extent in wild‐type than in γ229 cells. Both F9 cell lines showed a small stress‐dependent rise in [Ca2+]i levels and similar PKA‐c activity. In summary, the mechanical linkage of integrin‐vinculin‐cytoskeleton seemed not to be essential for chemical signal transduction.