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Register a new userTissue can generate propagating long-range forces on weakly adhesive substrate
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Cells in a tissue mutually coordinate their behaviors to maintain tissue homeostasis and control morphogenetic dynamics. As well as chemical signals, mechanical entities such as force and strain can be possible mediators of the signalling cues for this mutual coordination, but how such mechanical cues can propagate has not been fully understood. Here, we propose a mechanism of long-range force propagation through the extracellular matrix. We experimentally found a novel concentric wave of deformation in the elastic substrate underlying an epithelial monolayer around an extruding cell, under weakly-adhesive conditions which we define in our work. The deformation wave propagates over two cell sizes in ten minutes. The force transmission is revealed by the emergence of a pronounced peak in the deformation field of substrate. We derive a theoretical model based on linear elasticity theory, to analyse the substrate dynamics and to quantitatively validate this model. Through model analysis, we show that this propagation appears as a consequence of the stress exerted by the tissue on a soft substrate sliding on a stiff one. These results infer that the tissue can interact with embedding substrate with weakly adhesive structures to precisely transmit long-range forces for the regulation of a variety of cellular behaviors.
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Complex spatiotemporal patterns of action potential duration have been shown to occur in many mammalian hearts due to a period-doubling bifurcation that develops with increasing frequency of stimulation. Here, through high-resolution optical mapping and numerical simulations, we quantify voltage length scales in canine ventricles via spatiotemporal correlation analysis as a function of stimulation frequency and during fibrillation. We show that i) length scales can vary from 40 to 20 cm during one to one responses, ii) a critical decay length for the onset of the period-doubling bifurcation is present and decreases to less than 3 cm before the transition to fibrillation occurs, iii) fibrillation is characterized by a decay length of about 1 cm. On this evidence, we provide a novel theoretical description of cardiac decay lengths introducing an experimental-based conduction velocity dispersion relation that fits the measured wavelengths with a fractional diffusion exponent of 1.5. We show that an accurate phenomenological mathematical model of the cardiac action potential, fine-tuned upon classical restitution protocols, can provide the correct decay lengths during periodic stimulations but that a domain size scaling via the fractional diffusion exponent of 1.5 is necessary to reproduce experimental fibrillation dynamics. Our study supports the need of generalized reaction-diffusion approaches in characterizing the multiscale features of action potential propagation in cardiac tissue. We propose such an approach as the underlying common basis of synchronization in excitable biological media.
Adhesive cell-substrate interactions are crucial for cell motility and are responsible for the necessary traction that propels cells. These interactions can also change the shape of the cell, analogous to liquid droplet wetting on adhesive substrates. To address how these shape changes affect cell migration and cell speed we model motility using deformable, 2D cross-sections of cells in which adhesion and frictional forces between cell and substrate can be varied separately. Our simulations show that increasing the adhesion results in increased spreading of cells and larger cell speeds. We propose an analytical model which shows that the cell speed is inversely proportional to an effective height of the cell and that increasing this height results in increased internal shear stress. The numerical and analytical results are confirmed in experiments on motile eukaryotic cells.
Couplings between standard model particles and unparticles from a nontrivial scale invariant sector can lead to long range forces. If the forces couple to quantities such as baryon or lepton (electron) number, stringent limits result from tests of the gravitational inverse square law. These limits are much stronger than from collider phenomenology and astrophysics.
In embryonic development, programmed cell shape changes are essential for building functional organs, but in many cases the mechanisms that precisely regulate these changes remain unknown. We propose that fluid-like drag forces generated by the motion of an organ through surrounding tissue could generate changes to its structure that are important for its function. To test this hypothesis, we study the zebrafish left-right organizer, Kupffers vesicle (KV), using experiments and mathematical modeling. During development, monociliated cells that comprise the KV undergo region-specific shape changes along the anterior-posterior axis that are critical for KV function: anterior cells become long and thin, while posterior cells become short and squat. Here, we develop a mathematical vertex-like model for cell shapes, which incorporates both tissue rheology and cell motility, and constrain the model parameters using previously published rheological data for the zebrafish tailbud [Serwane et al.] as well as our own measurements of the KV speed. We find that drag forces due to dynamics of cells surrounding the KV could be sufficient to drive KV cell shape changes during KV development. More broadly, these results suggest that cell shape changes could be driven by dynamic forces not typically considered in models or experiments.
We describe a 3D percolation-type approach to modeling of the processes of aging and certain other properties of tissues analyzed as systems consisting of interacting cells. Lattice sites are designated as regular (healthy) cells, senescent cells, or vacancies left by dead (apoptotic) cells. The system is then studied dynamically with the ongoing processes including regular cell dividing to fill vacant sites, healthy cells becoming senescent or dying, and senescent cells dying. Statistical-mechanics description can provide patterns of time dependence and snapshots of morphological system properties. The developed theoretical modeling approach is found not only to corroborate recent experimental findings that inhibition of senescence can lead to extended lifespan, but also to confirm that, unlike 2D, in 3D senescent cells can contribute to tissues connectivity/mechanical stability. The latter effect occurs by senescent cells forming the second infinite cluster in the regime when the regular (healthy) cells infinite cluster still exits.
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