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Register a new userPico-Newton mechanical forces promote neurite growth
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Investigations over half a century have indicated that mechanical forces induce neurite growth - with neurites elongating at a rate of 0.1-0.3{mu}mh^{-1} per pico-Newton (pN) of applied force - when mechanical tension exceeds a threshold, with this being identified as 400-1000 pN for neurites of PC12 cells. Here we demonstrate that there is no threshold for neurite elongation of PC12 cells in response to applied mechanical forces. Instead, this proceeds at the same previously identified rate, on the application of tensions with intensity below 1pN. This supports the idea of mechanical tension as an endogenous signal used by neurons for promoting neurite elongation.
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Mechanics has an important role during morphogenesis, both in the generation of forces driving cell shape changes and in determining the effective material properties of cells and tissues. Drosophila dorsal closure (DC) has emerged as a model system for studying the interplay between tissue mechanics and cellular activity. Thereby, the amnioserosa (AS) generates one of the major forces that drive DC through the apical contraction of its constituent cells. We combined quantitation of live data, genetic and mechanical perturbation and cell biology, to investigate how mechanical properties and contraction rate emerge from cytoskeletal activity. We found that a decrease in Myosin phosphorylation induces a fluidization of AS cells which become more compliant. Conversely, an increase in Myosin phosphorylation and an increase in actin linear polymerization induce a solidification of cells. Contrary to expectation, these two perturbations have an opposite effect on the strain rate of cells during DC. While an increase in actin polymerization increases the contraction rate of AS cells, an increase in Myosin phosphorylation gives rise to cells that contract very slowly. The quantification of how the perturbation induced by laser ablation decays throughout the tissue revealed that the tissue in these two mutant backgrounds reacts very differently. We suggest that the differences in the strain rate of cells in situations where Myosin activity or actin polymerization is increased arise from changes in how the contractile forces are transmitted and coordinated across the tissue through ECadherin mediated adhesion. Our results show that there is an optimal level of Myosin activity to generate efficient contraction and suggest that the architecture of the actin cytoskeleton and the dynamics of adhesion complexes are important parameters for the emergence of coordinated activity throughout the tissue.
Advances in synthetic biology allow us to engineer bacterial collectives with pre-specified characteristics. However, the behavior of these collectives is difficult to understand, as cellular growth and division as well as extra-cellular fluid flow lead to complex, changing arrangements of cells within the population. To rationally engineer and control the behavior of cell collectives we need theoretical and computational tools to understand their emergent spatiotemporal dynamics. Here, we present an agent-based model that allows growing cells to detect and respond to mechanical interactions. Crucially, our model couples the dynamics of cell growth to the cells environment: Mechanical constraints can affect cellular growth rate and a cell may alter its behavior in response to these constraints. This coupling links the mechanical forces that influence cell growth and emergent behaviors in cell assemblies. We illustrate our approach by showing how mechanical interactions can impact the dynamics of bacterial collectives growing in microfluidic traps.
In this work, we study the in-vitro dynamics of the most malignant form of the primary brain tumor: Glioblastoma Multiforme. Typically, the growing tumor consists of the inner dense proliferating zone and the outer less dense invasive region. Experiments with different types of cells show qualitatively different behavior. Wild-type cells invade a spherically symmetric manner, but mutant cells are organized in tenuous branches. We formulate a model for this sort of growth using two coupled reaction-diffusion equations for the cell and nutrient concentrations. When the ratio of the nutrient and cell diffusion coefficients exceeds some critical value, the plane propagating front becomes unstable with respect to transversal perturbations. The instability threshold and the full phase-plane diagram in the parameter space are determined. The results are in a good agreement with experimental findings for the two types of cells.
Cell internalization of a blastomere, namely gastrulation, is a common and significant milestone during development of metazoans from worm to human, which generates multiple embryonic layers with distinct cell fates and spatial organizations. Although many molecular activities (e.g., cell polarization, asymmetrical intercellular adhesion, and apical actomyosin cortex contraction) have been revealed to facilitate this morphogenetic process, in this paper, we focus on gastrulation of the worm Caenorhabditis elegans and demonstrate that even a simple mechanical system, like a group of cells with isotropic repulsive and attractive interactions, can experience such internalization behavior spontaneously when dividing within a confined space. In principle, when the total cell number exceeds a threshold, a double-layer structure acquires lower potential energy and longer neighbor distance than the single-layer one. Besides, both mechanical analysis and simulation suggest that the cells with a large size or placed near a small-curvature boundary are easier to internalize. Last but not least, extra regulation on a limited part of cells to internalize autonomously can stabilize this process against motional noise. Our work successfully recaptures many key characteristics in worm gastrulation by mechanical modeling and provides a novel and rational interpretation on how this phenomenon emerges and is optimally programed.
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