期刊
JOURNAL OF CELL SCIENCE
卷 116, 期 8, 页码 1617-1625出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.00340
关键词
myosin II; cell spreading; cell mechanics; traction force; contraction; cytochalasin D
类别
资金
- NHLBI NIH HHS [HL-45788] Funding Source: Medline
- NIGMS NIH HHS [GM-38838] Funding Source: Medline
As it migrates over a substratum, a cell must exert different kinds of forces that act at various cellular locations and at specific times. These forces must therefore be coordinately regulated. The Rho-family GTPases Rac1 and Cdc42 promote actin polymerization that drives extension of the leading cell edge. Subsequently, RhoA regulates myosin-dependent contractile force, which is required for formation of adhesive contacts and stress fibers. During cell spreading, however, the activity of RhoA is reduced by a mechanism involving the tyrosine kinases c-Src and focal adhesion kinase (FAK), and the p190RhoGAP. It has been proposed that this reduction of RhoA activity facilitates edge extension by reducing myosin-dependent contractile forces that could resist this process. We have directly tested this hypothesis by correlating myosin activity with the rate of cell spreading on a substratum. The rate of spreading is inversely related to the myosin activity. Furthermore, spreading is inhibited by low concentrations of cytochalasin D, as expected for a process that depends on the growth of uncapped actin filaments. Cell indentation measurements show that a myosin-dependent viscoelastic force resists cell deformation.
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