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Treatment of epithelial African green monkey kidney (BSC-1) cells with the potent tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) induces a rapid and reversible redistribution of actin and vinculin that is detectable after only 2 min of treatment. Within 20-40 min, stress fibers disappear, while at the same time large actin-containing ribbons resembling ruffles develop both at the cell periphery and in more central regions. Vinculin is associated with these actin ribbons or bands in a punctate or patchy staining pattern. Adhesion to the substratum is changed from predominantly focal contacts associated with stress fiber ends in untreated cells to broad zones of close contact after TPA treatment. High voltage electron microscopic observations disclose the ribbons to consist of highly cross-linked actin filament networks. Thus, association of vinculin with filament networks, rather than (the ends of) filament bundles, is demonstrated. The integrity of microtubules and vimentin filaments is not affected by TPA treatment, but their distribution is altered to conform with the highly distorted cell shape. The response to TPA is neither prevented nor modified by nocodazole-induced depolymerization or taxol-induced stabilization of microtubules. An intact intermediate filament network seems not required either since colcemid-induced collapse of vimentin filaments towards the nucleus does not affect the cell's response to TPA. Rapid redistribution of actin and vinculin also takes place in enucleated cells and in the presence of cycloheximide, but is prevented by dinitrophenol or oligomycin. TPA-induced cytoskeletal alterations are independent of fibronectin expression and not mimicked, modified, or prevented by calmodulin inhibitors or experimentally elevated levels of calcium and cyclic AMP. Thus the morphological response to TPA involves rapid redistribution of actin and vinculin independent of transcription and translation, fluctuations in the levels of calcium or cyclic AMP, or changes in the organization of microtubules, intermediate filaments, and fibronectin.
M Schliwa, and
T Nakamura, and
K R Porter, and
U Euteneuer
January 1988,
Experimental cell research,
M Schliwa, and
T Nakamura, and
K R Porter, and
U Euteneuer
January 1988,
Proceedings of the National Academy of Sciences of the United States of America,
M Schliwa, and
T Nakamura, and
K R Porter, and
U Euteneuer
January 1983,
Cell motility,
M Schliwa, and
T Nakamura, and
K R Porter, and
U Euteneuer
March 1992,
The Journal of pathology,
M Schliwa, and
T Nakamura, and
K R Porter, and
U Euteneuer
May 1986,
Nippon Ganka Gakkai zasshi,
M Schliwa, and
T Nakamura, and
K R Porter, and
U Euteneuer
November 1991,
Journal of cell science,
M Schliwa, and
T Nakamura, and
K R Porter, and
U Euteneuer
January 1990,
Journal of ocular pharmacology,
M Schliwa, and
T Nakamura, and
K R Porter, and
U Euteneuer
January 2006,
Neoplasma,
M Schliwa, and
T Nakamura, and
K R Porter, and
U Euteneuer
April 2004,
Plant physiology,
M Schliwa, and
T Nakamura, and
K R Porter, and
U Euteneuer
January 2001,
Toxicon : official journal of the International Society on Toxinology,
