Filament sliding in simulations of CaMKII-actin bundles

Neuronal synapses form in the brain when the axons of presynaptic neurons connect to the dendrites of postsynaptic neurons. During the synapse formation, small protrusions form on the dendrites of the presynaptic neurons, called dendritic spines, after stimulation with high-frequency electric signals in a process known as long-term potentiation. Calcium/calmodulin-dependent protein kinase II (CaMKII) is crucial in long-term potentiation because it can decode signals, initiate phosphorylation cascades, and interact with actin filaments to form blunt-ended bundles. We modeled CaMKII-actin bundles using a coarse-grained model of four particles per actin promoter and a docking simulation performed in our group. We show that the geometry of CaMKII allows it to slide easily along actin filaments compared to other crosslinkers such as α-actinin and fascin. We also show that the sliding of CaMKII depends on the affinity and properties of the CaMKII-actin docking arrangement. Finally, we propose a mechanism that explains how CaMKII sliding leads to the formation of blunt-ended actin bundles.