English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Criticality in cell adhesion

MPS-Authors
/persons/resource/persons246176

Blom,  K.
Department of Theoretical and Computational Biophysics, MPI for Biophysical Chemistry, Max Planck Society;

/persons/resource/persons206062

Godec,  A.
Research Group of Mathematical Biophysics, MPI for Biophysical Chemistry, Max Planck Society;

External Resource
No external resources are shared
Fulltext (public)

3367134.pdf
(Publisher version), 2MB

Supplementary Material (public)
There is no public supplementary material available
Citation

Blom, K., & Godec, A. (2021). Criticality in cell adhesion. Physical Review X, 11(3): 031067. doi:10.1103/PhysRevX.11.031067.


Cite as: http://hdl.handle.net/21.11116/0000-0009-F605-C
Abstract
We illuminate the many-body effects underlying the structure, formation, and dissolution of cellular adhesion domains in the presence and absence of forces. We consider mixed Glauber-Kawasaki dynamics of a two-dimensional model of nearest-neighbor-interacting adhesion bonds with intrinsic binding affinity under the action of a shared pulling or pushing force. We consider adhesion bonds that are immobile due to being anchored to the underlying cytoskeleton, as well as adhesion molecules that are transiently diffusing. Highly accurate analytical results are obtained on the pair-correlation level of the Bethe-Guggenheim approximation for the complete thermodynamics and kinetics of adhesion clusters of any size, including the thermodynamic limit. A new kind of dynamical phase transition is uncovered—the mean formation and dissolution times per adhesion bond change discontinuously with respect to the bond-coupling parameter. At the respective critical points, cluster formation and dissolution are the fastest, while the statistically dominant transition path undergoes a qualitative change—the entropic barrier to a completely bound or unbound state is rate-limiting below, and the phase transition between dense and dilute phases above the dynamical critical point. In the context of the Ising model, the dynamical phase transition reflects a first-order discontinuity in the magnetization-reversal time. Our results provide a potential explanation for the mechanical regulation of cell adhesion and suggest that the quasistatic and kinetic responses to changes in the membrane stiffness or applied forces is largest near the statical and dynamical critical points, respectively.