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Cellular geometry regulates traction stresses (479.4)
Author(s) -
Oakes Patrick,
Banerjee Shiladitya,
Marchetti M. Cristina,
Gardel Margaret
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.479.4
Subject(s) - traction (geology) , focal adhesion , tractive force , cytoskeleton , stiffness , myosin , biophysics , materials science , actin , cell migration , curvature , tension (geology) , actin cytoskeleton , cell function , cell , mechanics , geometry , chemistry , composite material , physics , compression (physics) , biology , mathematics , paleontology , biochemistry , thermodynamics
Cells generate mechanical stresses via the action of myosin motors on the actin cytoskeleton. While the molecular origin of force generation is well understood, we currently lack an understanding of the regulation of force transmission at cellular length scales. Here we experimentally decouple the effects of substrate stiffness, focal adhesion density and cell morphology to show that the total amount of work a cell does against the substrate to which it is adhered is regulated by the cell spread area alone. Surprisingly, the number of focal adhesions and the substrate stiffness have little effect on regulating the work done on the substrate by the cell. For a given spread area, the local curvature along the cell edge regulates the distribution and magnitude of traction stresses to maintain a constant strain energy. A physical model of the adherent cell as a contractile gel under a uniform boundary tension and mechanically coupled to an elastic substrate quantitatively captures the spatial distribution and magnitude of traction stresses. With a single choice of parameters, this model accurately predicts the cell's mechanical output as a function of cell geometry. Grant Funding Source : Supported by the NSF, NIH and the Burroughs Wellcome Fund.