The architecture and geometry of the actin networks are tightly controlled in these essential cellular processes, and defects in this control cause pathologies, such as ageing disorders ( Amberg et al., 2011). Introductionĭynamic actin networks play important roles in cell migration ( Rottner and Stradal, 2011), morphogenesis ( Hopmann and Miller, 2003), immune response ( Vargas et al., 2016) and intracellular pathogen motility ( Reed et al., 2014). Our results establish general principles on how the dynamic steady state of actin network emerges from biochemical and structural feedbacks. Selective disassembly of heterogeneous networks by ADF/Cofilin controls steering during motility. A single rate of breaking network nodes, proportional to ADF/Cofilin density and inversely proportional to the square of the actin density, can account for the disassembly dynamics. Local depletion of ADF/Cofilin by binding to actin is significant, leading to wider networks growing longer. A mathematical model predicts the network length as a function of width, actin and ADF/Cofilin concentrations. At the trailing edge, the network disintegrated into large fragments. In the presence of ADF/Cofilin, networks reached equilibrium and became treadmilling.
Using both in vitro and in silico approaches, we studied the effect of key parameters, such as actin density, ADF/Cofilin concentration and network width on the network length. Principles of regulation of actin network dimensions are fundamentally important for cell functions, yet remain unclear.
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