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• W1998063139 abstract "Cell adhesion and motility depend strongly on the interactions between cells and extracellular matrix (ECM) substrates. When plated onto artificial adhesive surfaces, cells first flatten and deform extensively as they spread. At the molecular level, the interaction of membrane-based integrins with the ECM has been shown to initiate a complex cascade of signaling events [1Zamir E. Geiger B. Components of cell-matrix adhesions.J. Cell Sci. 2001; 114: 3577-3579Crossref PubMed Google Scholar], which subsequently triggers cellular morphological changes and results in the generation of contractile forces [2Balaban N.Q. Schwarz U.S. Riveline D. Goichberg P. Tzur G. Sabanay I. Mahalu D. Safran S. Bershadsky A. Addadi L. et al.Force and focal adhesion assembly: A close relationship studied using elastic micro-patterned substrates.Nat. Cell Biol. 2001; 3: 466-472Crossref PubMed Scopus (1669) Google Scholar]. Here, we focus on the early stages of cell spreading and probe their dynamics by quantitative visualization and biochemical manipulation with a variety of cell types and adhesive surfaces, adhesion receptors, and cytoskeleton-altering drugs. We find that the dynamics of adhesion follows a universal power-law behavior. This is in sharp contrast with the common belief that spreading is regulated by either the diffusion of adhesion receptors toward the growing adhesive patch [3Dustin M.L. Ferguson L.M. Chan P.Y. Springer T.A. Golan D.E. Vizualization of CD2 interaction with LFA-3 and determination of the two-dimensional dissociation constant for adhesion receptors in a contact area.J. Cell Biol. 1996; 132: 465-477Crossref PubMed Scopus (193) Google Scholar, 4Yauch R.L. Felsenfeld D.P. Kraeft S.K. Chen L.B. Sheetz M.P. Hemler M.E. Mutational evidence for control of cell adhesion through integrin diffusion/clustering, independent of ligand binding.J. Exp. Med. 1997; 186: 1347-1355Crossref PubMed Scopus (142) Google Scholar, 5Shenoy V.B. Freund L.B. Growth and shape stability of a biological membrane adhesion complex in the diffusion-mediated regime.Proc. Natl. Acad. Sci. USA. 2005; 102: 3213-3218Crossref PubMed Scopus (73) Google Scholar] or by actin polymerization [6Chamaraux F. Fache S. Bruckert F. Fourcade B. Kinetics of cell spreading.Phys. Rev. Lett. 2005; 94: 158102Crossref PubMed Scopus (43) Google Scholar, 7Bereiter-Hahn J. Lück M. Miebach T. Stelzer H.K. Vöth M. Spreading of trypsinized cells: Cytoskeletal dynamics and energy requirements.J. Cell Sci. 1990; 96: 171-188Crossref PubMed Google Scholar, 8Cai Y. Biais N. Gianone G. Tanase M. Ladoux B. Hofman J. Wiggins C.H. Sheetz M.P. Nonmuscle myosin IIA-dependent force inhibits cell spreading and drives F-actin flow.Biophys. J. 2006; 91: 3907-3920Abstract Full Text Full Text PDF PubMed Scopus (217) Google Scholar]. To explain this, we propose a simple quantitative and predictive theory that models cells as viscous adhesive cortical shells enclosing a less viscous interior. Thus, although cell spreading is driven by well-identified biomolecular interactions, it is dynamically limited by its mesoscopic structure and material properties." @default.
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• W1998063139 date "2007-04-01" @default.
• W1998063139 modified "2023-10-16" @default.
• W1998063139 title "The Universal Dynamics of Cell Spreading" @default.
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• W1998063139 doi "https://doi.org/10.1016/j.cub.2007.02.058" @default.
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