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Register a new userModel for Osteosarcoma-9 as a Potent Factor in Cell Survivor and Resistance to Apoptosis
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In this paper we use a simple toy model to explore the function of the gene Osteosarcoma-9. We are in particular interested in understanding the role of this gene as a potent anti-apoptotic factor. The theoretical description is constrained by experimental data from induction of apoptosis in cells where OS-9 is overexpressed. The data available suggest that OS-9 promotes cell viability and confers resistance to apoptosis, potentially implicating OS-9 in the survival of cancer cells. Three different apoptosis inducing mechanisms were tested and are here modelled. More complex and realistic models are also discussed.
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Biochemistry and mechanics are closely coupled in cell adhesion. At sites of cell-matrix adhesion, mechanical force triggers signaling through the Rho-pathway, which leads to structural reinforcement and increased contractility in the actin cytoskeleton. The resulting force acts back to the sites of adhesion, resulting in a positive feedback loop for mature adhesion. Here we model this biochemical-mechanical feedback loop for the special case when the actin cytoskeleton is organized in stress fibers, which are contractile bundles of actin filaments. Activation of myosin II molecular motors through the Rho-pathway is described by a system of reaction-diffusion equations, which are coupled into a viscoelastic model for a contractile actin bundle. We find strong spatial gradients in the activation of contractility and in the corresponding deformation pattern of the stress fiber, in good agreement with experimental findings.
Genetically identical cells under the same environmental conditions can show strong variations in protein copy numbers due to inherently stochastic events in individual cells. We here develop a theoretical framework to address how variations in enzyme abundance affect the collective kinetics of metabolic reactions observed within a population of cells. Kinetic parameters measured at the cell population level are shown to be systematically deviated from those of single cells, even within populations of homogeneous parameters. Because of these considerations, Michaelis-Menten kinetics can even be inappropriate to apply at the population level. Our findings elucidate a novel origin of discrepancy between in vivo and in vitro kinetics, and offer potential utility for analysis of single-cell metabolomic data.
We develop a theoretical approach that uses physiochemical kinetics modelling to describe cell population dynamics upon progression of viral infection in cell culture, which results in cell apoptosis (programmed cell death) and necrosis (direct cell death). Several model parameters necessary for computer simulation were determined by reviewing and analyzing available published experimental data. By comparing experimental data to computer modelling results, we identify the parameters that are the most sensitive to the measured system properties and allow for the best data fitting. Our model allows extraction of parameters from experimental data and also has predictive power. Using the model we describe interesting time-dependent quantities that were not directly measured in the experiment, and identify correlations among the fitted parameter values. Numerical simulation of viral infection progression is done by a rate-equation approach resulting in a system of stiff equations, which are solved by using a novel variant of the stochastic ensemble modelling approach. The latter was originally developed for coupled chemical reactions.
The interaction between actin filaments and microtubules is crucial for many eukaryotic cellular processes, such as, among others, cell polarization, cell motility and cellular wound healing. The importance of this interaction has long been recognised, yet very little is understood about both the underlying mechanisms and the consequences for the spatial (re)organization of the cellular cytoskeleton. At the same time, understanding the causes and the consequences of the interaction between different biomolecular components are key questions for emph{in vitro} research involving reconstituted biomolecular systems, especially in the light of current interest in creating minimal synthetic cells. In this light, recent emph{in vitro} experiments have shown that the actin-microtubule interaction mediated by the cytolinker TipAct, which binds to actin lattice and microtubule tip, causes the directed transport of actin filaments. We develop an analytical theory of dynamically unstable microtubules, nucleated from the center of a spherical cell, in interaction with actin filaments. We show that, depending on the balance between the diffusion of unbound actin filaments and propensity to bind microtubules, actin is either concentrated in the center of the cell, where the density of microtubules is highest, or becomes localized to the cell cortex.
Extraordinarily large but short electric field pulses are reported by many experiments to cause bipolar cancellation (BPC). This unusual cell response occurs if a first pulse is followed by a second pulse with opposite polarity. Possibly universal, BPC presently lacks a mechanistic explanation. Multipl
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