Adaptive flexibility of cells through nonequilibrium entropy production

Cellular adaptation to environmental changes relies on the dynamic remodeling of subcellular structures. Among these, periodic actomyosin assemblies are fundamental to the organization and function of the cytoskeletal architecture. In muscle-type cells, sarcomeres exhibit ordered structures of consistent lengths, optimized for stable force generation. By contrast, nonmuscle-type cells exhibit greater structural variability, with sarcomere-like periodic units of varying lengths that contribute not only to force generation but also to adaptive remodeling upon environmental cues. These structural differences have traditionally been attributed to the specific protein compositions unique to each cell type. However, the functional significance of such periodic unit variability remains poorly understood within a unified framework. Here, we propose a conceptual model grounded in nonequilibrium physics to provide a unified perspective on structural variability in cytoskeletal adaptation. Specifically, we demonstrate that the effective binding strength of these contractile units can be evaluated by quantifying structural randomness through Shannon entropy. The increased entropy associated with the inherent randomness of sarcomere-like assemblies in nonmuscle-type cells lowers the energy barrier for cytoskeletal remodeling, enabling flexible adaptation to environmental demands. In contrast, the ordered sarcomere arrangements in muscle-type cells correspond to higher binding energies, stabilizing cytoskeletal configurations for sustained force generation. While structural disorder is often regarded as a source of instability, our analysis reveals that it can serve as a driver of cytoskeletal remodeling and a foundation for adaptive cellular behavior. Thus, our study provides a unified theoretical foundation for understanding cytoskeletal adaptability across diverse cell types by integrating structural randomness into a nonequilibrium framework.