The dual role of calcium/calmodulin-dependent kinase II in transducing calcium signals and reorganizing actomyosin networks

Calcium/calmodulin-dependent kinase II (CaMKII) plays a key role in the plasticity of dendritic spines. Calcium signals (Ca²⁺) cause calcium-calmodulin (CaM) to active CaMKII, which leads to remodeling of the actin filament network in the spine. In this presentation, I will first focus on the binding mechanism of CaM and its binding target, which requires mutually- and conformationally-induced changes in both participants Then, I will reveal how a target mechanistically tunes CaM’s affinity for Ca²⁺ by examining interactions with neurogranin (Ng) and CaM-dependent kinase II (CaMKII). These two targets are biochemically known to tune CaM’s affinity for Ca²⁺ in opposite directions in postsynaptic neuronal cells. I will further discuss the active role of holoenzyme CaM/CaMKII in transmitting chemical reactions at a molecular scale to specific mechanical responses at a micron scale by alternating the topology of actomyosin networks. The observation made by a team of collaborators using an integrated approach of experiments, theory, and computation provides a simple mechanism by which the structural dynamics of CaMKII establishes a link between calcium signaling and the morphological plasticity of dendritic spines.