  Transient networks comprised of polymers connected by short-lived bonds are a
common design theme for both biological and synthetic materials. Transient
bonds can provide mechanical rigidity, while still allowing for visco-elastic
flows on timescales longer than the bond lifetime. In many biological polymer
networks such as the actin cytoskeleton, the short-lived bonds are formed by
accessory proteins that diffuse away after unbinding. By contrast, bonds in
synthetic networks, such as the pendant groups of telechelic polymers, can only
rebind in the same location. Using a recently developed theoretical model of
the fracturing of visco-elastic materials, we here investigate the effect of
linker mobility on the bond dynamics of a network under stress. We find that
although mean field properties such as the average bond linker lifetime are
barely affected by bond mobility, networks cross linked by mobile bonds
fracture more readily due to 'leaking' of linkers from crack areas to less
stressed regions within the network. We propose a theoretical model to describe
the redistribution of mobile linkers, which we validate by simulations. Our
work offers insight into a potential trade-off that cells face, between
fracture strength versus the modularity and tight dynamic control offered by
mobile linkers.
