Crosslinker mobility weakens transient polymer networks

TL;DR

This paper investigates how the mobility of crosslinkers in transient polymer networks influences their fracture behavior, revealing that mobile linkers lead to easier fracture despite similar bond lifetimes.

Contribution

It introduces a theoretical model and simulations showing that linker mobility causes networks to fracture more readily due to linker redistribution.

Findings

Mobile linkers cause increased network fracture susceptibility.

Mean bond lifetime is unaffected by linker mobility.

Linker redistribution explains fracture behavior.

Abstract

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.