Abstract
It has been suggested that the polymerization of actin to form actin filaments is critical for many functions in non-muscle cells including phagocytosis, cell division, secretion and cell motility1,2. In support of this suggestion, many of these functions are inhibited by cytochalasins3 which also inhibit the actin nuclei-induced polymerization of purified actin4–7. Recent studies suggest that the cytochalasins (cytochalasins B, D and E) inhibit polymerization by binding to the growing end of actin filaments and blocking the further addition of monomeric actin molecules4,7–9. If the cytochalasins inhibit cellular contractile functions by a similar mechanism, they could be useful tools in determining whether actin polymerization is required for specific processes within cells. Blood platelets provide an excellent system for testing this as exposure of platelets to thrombin results in a rapid polymerization of actin10,11. We have now studied the effects of the cytochalasins on thrombin-induced actin polymerization and report here the first clear evidence that cytochalasins inhibit actin polymerization in intact cells.
Similar content being viewed by others
References
Clarke, M. & Spudich, J. A. A. Rev. Biochem. 46, 797–822 (1977).
Korn, E. D. Proc. natn. Acad. Sci. U.S.A. 75, 588–599 (1978).
Wessells, N. K. et al. Science 171, 135–143 (1971).
Brown, S. S. & Spudich, J. A. J. Cell Biol. 83, 657–662 (1979).
Lin, D. C. & Lin, S. Proc. natn. Acad. Sci. U.S.A. 76, 2345–2349 (1979).
Brenner, S. L. & Korn, E. D. J. biol. Chem. 255, 1670–1676 (1980).
MacLean-Fletcher, S. & Pollard, T. D. Cell 20, 329–341 (1980).
Brenner, S. L. & Korn, E. D. J. biol. Chem. 254, 9982–9985 (1979).
Flanagan, M. D. & Lin, S. J. biol. Chem. 255, 835–838 (1980).
Carlsson, L., Markey, F., Blikstad, I., Persson, T. & Lindberg, U. Proc. natn. Acad. Sci. U.S.A. 76, 6376–6380 (1979).
Phillips, D. R., Jennings, L. K. & Edwards, H. H. J. Cell Biol. 86, 77–86 (1980).
Blikstad, I., Markey, F., Carlsson, L., Persson, T. & Lindberg, U. Cell 15, 935–943 (1978).
Jennings, L. K., Fox, J. E. B., Edwards, H. H. & Phillips, D. R. J. biol. Chem. (in the press).
Kletzien, R. F., Perdue, J. F. & Springer, A. J. biol. Chem. 247, 2964–2966 (1972).
Plagemann, P. G. W. & Estensen, R. D. J. Cell Biol. 55, 179–185 (1972).
Lin, S. & Snyder, C. E. J. biol. Chem. 252, 5464–5471 (1977).
Lin, S., Santi, D. V. & Spudich, J. A. J. biol. Chem. 249, 2268–2274 (1974).
Rampal, A. L., Pinkofsky, H. B. & Jung, C. Y. Biochemistry 19, 679–683 (1980).
Lyons, R. M., Stanford, N. & Majerus, P. W. J. clin. Invest. 56, 924–936 (1975).
Wegner, A. J. molec. Biol. 108, 139–150 (1976).
Morris, A. & Tannenbaum, J. Nature 287, 637–639 (1980).
Swanston-Flatt, S. K., Carlsson, L. & Gylfe, E. FEBS Lett. 117, 299–302 (1980).
Howell, S. L. & Tyhurst, M. Biochem. J. 192, 381–383 (1980).
Phillips, D. R. & Agin, P. P. J. clin. Invest. 60, 535–545 (1977).
Pollard, T. D. & Mooseker, M. S. J. Cell Biol. 88, 654–659 (1981).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Fox, J., Phillips, D. Inhibition of actin polymerization in blood platelets by cytochalasins. Nature 292, 650–652 (1981). https://doi.org/10.1038/292650a0
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1038/292650a0
- Springer Nature Limited
This article is cited by
-
Fscn1 is required for the trafficking of TGF-β family type I receptors during endoderm formation
Nature Communications (2016)
-
Incorporation of Ophiobolin A into Novel Chemoembolization Particles for Cancer Cell Treatment
Pharmaceutical Research (2014)
-
Reduced levels of intracellular calcium releasing in spermatozoa from asthenozoospermic patients
Reproductive Biology and Endocrinology (2009)
-
Studies on the actin-binding protein HS1 in platelets
BMC Cell Biology (2007)
-
FcεRI cross‐linking‐induced actin assembly mediates calcium signalling in RBL‐2H3 mast cells
British Journal of Pharmacology (2002)