TY - JOUR
T1 - Physical model for self-organization of actin cytoskeleton and adhesion complexes at the cell front
AU - Shemesh, Tom
AU - Bershadsky, Alexander D.
AU - Kozlov, Michael M.
N1 - Funding Information:
Financial support for M.M.K. from the Israel Science Foundation and Marie Curie Network “Virus Entry” is gratefully acknowledged. A.D.B. holds the Joseph Moss Professorial Chair in Biomedical Research at the Weizmann Institute and is a Visiting Professor at the National University of Singapore, and acknowledges support from Israel Science Foundation, De Benedetti Foundation-Cherasco (Turin, Italy), and Mechanobiology Institute, National University of Singapore, Singapore. M.M.K. and T.S. are grateful to the Mechanobiology Institute (National University of Singapore) for its hospitality in July and November 2011.
PY - 2012/4/18
Y1 - 2012/4/18
N2 - Cell motion is driven by interplay between the actin cytoskeleton and the cell adhesions in the front part of the cell. The actin network segregates into lamellipodium and lamellum, whereas the adhesion complexes are characteristically distributed underneath the actin system. Here, we suggest a computational model for this characteristic organization of the actin-adhesion system. The model is based on the ability of the adhesion complexes to sense mechanical forces, the stick-slip character of the interaction between the adhesions and the moving actin network, and a hypothetical propensity of the actin network to disintegrate upon sufficiently strong stretching stresses. We identify numerically three possible types of system organization, all observed in living cells: two states in which the actin network exhibits segregation into lamellipodium and lamellum, whereas the cell edge either remains stationary or moves, and a state where the actin network does not undergo segregation. The model recovers the asynchronous fluctuations and outward bulging of the cell edge, and the dependence of the edge protrusion velocity on the rate of the nascent adhesion generation, the membrane tension, and the substrate rigidity.
AB - Cell motion is driven by interplay between the actin cytoskeleton and the cell adhesions in the front part of the cell. The actin network segregates into lamellipodium and lamellum, whereas the adhesion complexes are characteristically distributed underneath the actin system. Here, we suggest a computational model for this characteristic organization of the actin-adhesion system. The model is based on the ability of the adhesion complexes to sense mechanical forces, the stick-slip character of the interaction between the adhesions and the moving actin network, and a hypothetical propensity of the actin network to disintegrate upon sufficiently strong stretching stresses. We identify numerically three possible types of system organization, all observed in living cells: two states in which the actin network exhibits segregation into lamellipodium and lamellum, whereas the cell edge either remains stationary or moves, and a state where the actin network does not undergo segregation. The model recovers the asynchronous fluctuations and outward bulging of the cell edge, and the dependence of the edge protrusion velocity on the rate of the nascent adhesion generation, the membrane tension, and the substrate rigidity.
UR - http://www.scopus.com/inward/record.url?scp=84859902571&partnerID=8YFLogxK
U2 - 10.1016/j.bpj.2012.03.006
DO - 10.1016/j.bpj.2012.03.006
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AN - SCOPUS:84859902571
SN - 0006-3495
VL - 102
SP - 1746
EP - 1756
JO - Biophysical Journal
JF - Biophysical Journal
IS - 8
ER -