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Shadkhoo, S.

Publications and source records attributed to Shadkhoo, S..

2 recordsLinked to original sources

Force Propagation in Active Cytoskeletal Networks

Conventional materials science establishes clear structure-function relationships: grain boundaries modulate strength by blocking dislocations, and defect density limits conductivity through electron scattering. Active matter presents a fundamentally different challenge, components continuously consume energy to generate forces, creating a dual identity as both structural elements and force-generating machines. This material-machine duality raises a fundamental question: which structural parameters govern functional behavior in systems where constituents actively generate forces rather than merely responding to external inputs? Here we demonstrate that percolation is the critical mechanism that transforms active cytoskeletal networks from energy-dissipating materials into work-performing machines. Using light-controlled microtubule-kinesin networks, we show that increasing bundle length from 0.9 {micro}m to 5 {micro}m triggers a percolation transition that enables global force organization. Networks below the threshold remain incapable of performing coordinated work, while networks above it develop correlation lengths exceeding 240 {micro}m, generate 25-fold stronger forces, and extract 1000-fold more mechanical work, powering transport of live cells across 800 {micro}m distances. Network simulations reveal that introducing just 5-10% longer bundles creates a connected component containing 90% of microtubules, establishing the precise threshold that drives this material-to-machine transition. Our findings establish percolation as the fundamental mechanism governing whether active matter systems function as passive materials or as coordinated machines--providing design principles for both synthetic and biological systems. increasing bundle length from 0.9 {micro}m to 5 {micro}m increasing bundle length from 0.9 {micro}m to 5 {micro}m

biophysics↗

The Role of Cytoplasmic Interactions in the Collective Polarization of Tissues and its Interplay with Cellular Geometry

Planar cell polarity (PCP), the ability of a tissue to polarize coherently over multicellular length scales, provides the directional information that guides a multitude of developmental processes at cellular and tissue levels. While it is manifest that cells utilize both intra-cellular and intercellular mechanisms, how they couple together to produce the collective response remains an active area of investigation. Exploring a phenomeno-logical reaction-diffusion model, we predict a crucial, and novel, role for cytoplasmic interactions in the large-scale correlations of cell polarities. We demonstrate that finite-range (i.e. nonlocal) cytoplasmic interactions are necessary and sufficient for the robust and long-range polarization of tissues -- even in the absence of global cues -- and are essential to the faithful detection of weak directional signals. Strikingly, our model re-capitulates an observed influence of anisotropic tissue geometries on the orientation of polarity. In order to facilitate a conversation between theory and experiments, we compare five distinct classes of in silico mutants with experimental observations. Within this context, we propose quantitative measures that can guide the search for the participant molecular components, and the identification of their roles in the collective polarization of tissues.

biophysics↗