| The mechanical failure of a bioadhesion bond and that of a fluid biomembrane involve thermally-activated nucleation of critical-size defects: i.e. metastable separation between several interacting atomic-scale residues in the first case and metastable pore in the second case. As such, the stablilities of weak bioadhesion bonds and biomembrane vesicles are determined by energy barriers that gate the defect excitations. When external mechanical stress couples to a defect pathway and lowers the activation barrier, the frequency of failure increases enormously. For example, tensile stresses increase failure rates of bioadhesion bonds and biomembranes by several orders of magnitude in laboratory experiments revealing how the critical defect size changes with stress. Consistent with the mesoscopic mechanics of opening a hole in a 2-D fluid film, the failure rates measured for tense lipid bilayer vesicles show that the critical defect size diminishes progressively with increase in stress. On the other hand, the failure rates measured for integrin bioadhesion bonds indicate that defect size remains constant under pulling forces even though the increase in failure frequency implies >10 kBT reduction in the activation energy barrier. Although unexpected in the context of idealized physical theory, the constant defect size suggests that the macromolecular bonds separate by some type of "brittle" fracture process under stress. Prototypical of many bioadhesion complexes in eukaryote biology, the peculiar kinetics of failure are likely related to the dynamics of mesoscopic contact between stiff macromolecule surfaces mediated by numerous very weak interactions spread over 100's of Å2. |
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