arXiv subjects

Yuika Ueda

Publications and source records attributed to Yuika Ueda.

3 recordsLinked to original sources

arXiv2024

Adaptive flexibility of cells through nonequilibrium entropy production

Cellular adaptation to environmental changes relies on the dynamic remodeling of subcellular structures. Among these, sarcomere structures 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 display a higher degree of structural variability, with sarcomeres of varying lengths that contribute not only to force generation but also to adaptive remodeling upon environmental cues. While these differences in sarcomere structures have traditionally been attributed to the unique properties of specific proteins expressed in each cell type, the functional implications of such structural variability remain unclear. Here, we present a nonequilibrium physics framework to elucidate the role of sarcomere variability in cytoskeletal adaptation. Specifically, we demonstrate that the effective binding strength of sarcomere components can be evaluated by analyzing structural randomness using Shannon entropy. The increased entropy associated with the inherent randomness of sarcomere structures in nonmuscle-type cells lowers the energy barrier for cytoskeletal remodeling, enabling flexible adaptation to environmental demands. Meanwhile, the ordered sarcomere arrangements in muscle-type cells correspond to higher binding energies and more stable cytoskeletal configurations. Although structural disorder is often regarded as unfavorable in terms of stability, our study suggests that it plays a key role in enabling adaptive responses in cellular systems.

q-bio.CB↗

arXiv2024

A statistical-mechanical framework for mechanically adaptive cytoskeletal organization

Living cells continuously remodel their cytoskeleton in response to mechanical cues. Although these responses have been extensively documented, it remains unclear why continuous changes in the mechanical environment give rise to distinct intracellular architectures rather than gradual structural variation. Here, we introduce a statistical-mechanical framework in which alternative cytoskeletal organizations are represented as ensembles of microscopic configurations, allowing configurational entropy to compete with mechanically dependent interaction energies. Rather than reproducing the full molecular complexity of the cytoskeleton, the model asks which features of mechanically adaptive organization emerge from this minimal physical description. The framework predicts three successive structural transitions corresponding to stress fiber formation, alignment, and lateral aggregation. When these transitions are placed on a common cellular-tension axis that increases with substrate stiffness, the predicted sequence is consistent with our measurements of correlation length and anisotropy in senescent fibroblasts. The preservation of this stiffness-dependent sequence despite altered cellular physiology suggests that the observed ordering reflects a robust physical principle rather than a cell-state-specific phenomenon. Together, these results establish a statistical-mechanical framework for understanding how continuous mechanical cues bias the statistical selection of distinct cytoskeletal architectures.

q-bio.CB↗

arXiv2024

Scale-dependent physical constraints on active intracellular fluctuations

Living cells exhibit nonequilibrium dynamics that shape intracellular processes across length scales, from nanoscale molecular assembly to the organization of macroscopic organelles. While dynamics at micrometer scales are known to be constrained by the actin meshwork at low frequencies, the physical principles governing active fluctuations at the nanoscale remain elusive. Here, we present an analytical framework integrating fluorescence correlation spectroscopy with nonequilibrium modeling to delineate the physical scaling of intracellular mechanics. Applying this framework to fibroblasts, we demonstrate that, in contrast to larger components, nanoscale active fluctuations remain prominent at high frequencies and are predominantly driven by local nonmuscle myosin II activity, establishing a distinct functional hierarchy in intracellular mechanics: local active forces promote rapid spatial exploration for nanoscale molecules, whereas macroscopic actin constraints ensure the structural stability required for larger molecular complexes and organelles. To integrate these scale-dependent behaviors within a single physical framework, we formulated a model that captures the transition of active fluctuations across length scales, revealing that the physical properties of the cytoplasm are governed by the balance between active driving forces and passive structural constraints. Furthermore, applying this model to cellular senescence reveals a reduction in nonequilibrium complexity associated with cytoskeletal rigidification. Thus, our findings bridge the dimensional gap between local molecular kinetics and macroscopic constraints, providing a fundamental physical basis for understanding the hierarchical organization of intracellular dynamics.

physics.bio-ph↗