2,426 research outputs found
Mathematical modelling and numerical simulations of actin dynamics in the eukaryotic cell
The aim of this article is to study cell deformation and cell movement by considering both the mechanical and biochemical properties of the cortical network of actin filaments and its concentration. Actin is a polymer that can exist either in fil- amentous form (F-actin) or in monometric form (G-actin) (Chen et al. 2000) and the filamentous form is arranged in a paired helix of two protofilaments (Ananthakrish- nan et al. 2006). By assuming that cell deformations are a result of the cortical actin dynamics in the cell cytoskeleton, we consider a continuum mathematical model that couples the mechanics of the network of actin filaments with its bio-chemical dy- namics. Numerical treatment of the model is carried out using the moving grid finite element method (Madzvamuse et al. 2003). Furthermore, by assuming slow deforma- tions of the cell, we use linear stability theory to validate the numerical simulation results close to bifurcation points. Far from bifurcation points, we show that the math- ematical model is able to describe the complex cell deformations typically observed in experimental results. Our numerical results illustrate cell expansion, cell contrac- tion, cell translation and cell relocation as well as cell protrusions. In all these results, the contractile tonicity formed by the association of actin filaments to the myosin II motor proteins is identified as a key bifurcation parameter
On the Properties of a Bundle of Flexible Actin Filaments in an Optical Trap
We establish the Statistical Mechanics framework for a bundle of Nf living
and uncrosslinked actin filaments in a supercritical solution of free monomers
pressing against a mobile wall. The filaments are anchored normally to a fixed
planar surface at one of their ends and, because of their limited flexibility,
they grow almost parallel to each other. Their growing ends hit a moving
obstacle, depicted as a second planar wall, parallel to the previous one and
subjected to a harmonic compressive force. The force constant is denoted as
trap strength while the distance between the two walls as trap length to make
contact with the experimental optical trap apparatus. For an ideal solution of
reactive filaments and free monomers at fixed free monomers chemical potential,
we obtain the general expression for the grand potential from which we derive
averages and distributions of relevant physical quantities, namely the obstacle
position, the bundle polymerization force and the number of filaments in direct
contact with the wall. The grafted living filaments are modeled as discrete
Wormlike chains, with Factin persistence length, subject to discrete contour
length variations to model single monomer (de)polymerization steps. Rigid
filaments, either isolated or in bundles, all provide average values of the
stalling force in agreement with Hill's predictions, independent of the average
trap length. Flexible filaments instead, for values of the trap strength
suitable to prevent their lateral escape, provide an average bundle force and
an average trap length slightly larger than the corresponding rigid cases (few
percents). Still the stalling force remains nearly independent on the average
trap length, but results from the product of two strongly L dependent
contributions: the fraction of touching filaments and the single filament
buckling force.Comment: 21 pages, 8 figure
On the Nature and Shape of Tubulin Trails: Implications on Microtubule Self-Organization
Microtubules, major elements of the cell skeleton are, most of the time, well
organized in vivo, but they can also show self-organizing behaviors in time
and/or space in purified solutions in vitro. Theoretical studies and models
based on the concepts of collective dynamics in complex systems,
reaction-diffusion processes and emergent phenomena were proposed to explain
some of these behaviors. In the particular case of microtubule spatial
self-organization, it has been advanced that microtubules could behave like
ants, self-organizing by 'talking to each other' by way of hypothetic (because
never observed) concentrated chemical trails of tubulin that are expected to be
released by their disassembling ends. Deterministic models based on this idea
yielded indeed like-looking spatio-temporal self-organizing behaviors.
Nevertheless the question remains of whether microscopic tubulin trails
produced by individual or bundles of several microtubules are intense enough to
allow microtubule self-organization at a macroscopic level. In the present
work, by simulating the diffusion of tubulin in microtubule solutions at the
microscopic scale, we measure the shape and intensity of tubulin trails and
discuss about the assumption of microtubule self-organization due to the
production of chemical trails by disassembling microtubules. We show that the
tubulin trails produced by individual microtubules or small microtubule arrays
are very weak and not elongated even at very high reactive rates. Although the
variations of concentration due to such trails are not significant compared to
natural fluctuations of the concentration of tubuline in the chemical
environment, the study shows that heterogeneities of biochemical composition
can form due to microtubule disassembly. They could become significant when
produced by numerous microtubule ends located in the same place. Their possible
formation could play a role in certain conditions of reaction. In particular,
it gives a mesoscopic basis to explain the collective dynamics observed in
excitable microtubule solutions showing the propagation of concentration waves
of microtubules at the millimeter scale, although we doubt that individual
microtubules or bundles can behave like molecular ants
Modelling cell motility and chemotaxis with evolving surface finite elements
We present a mathematical and a computational framework for the modelling of cell motility. The cell membrane is represented by an evolving surface, with the movement of the cell determined by the interaction of various forces that act normal to the surface. We consider external forces such as those that may arise owing to inhomogeneities in the medium and a pressure that constrains the enclosed volume, as well as internal forces that arise from the reaction of the cells' surface to stretching and bending. We also consider a protrusive force associated with a reaction-diffusion system (RDS) posed on the cell membrane, with cell polarization modelled by this surface RDS. The computational method is based on an evolving surface finite-element method. The general method can account for the large deformations that arise in cell motility and allows the simulation of cell migration in three dimensions. We illustrate applications of the proposed modelling framework and numerical method by reporting on numerical simulations of a model for eukaryotic chemotaxis and a model for the persistent movement of keratocytes in two and three space dimensions. Movies of the simulated cells can be obtained from http://homepages.warwick.ac.uk/maskae/CV_Warwick/Chemotaxis.html
Molecular motors robustly drive active gels to a critically connected state
Living systems often exhibit internal driving: active, molecular processes
drive nonequilibrium phenomena such as metabolism or migration. Active gels
constitute a fascinating class of internally driven matter, where molecular
motors exert localized stresses inside polymer networks. There is evidence that
network crosslinking is required to allow motors to induce macroscopic
contraction. Yet a quantitative understanding of how network connectivity
enables contraction is lacking. Here we show experimentally that myosin motors
contract crosslinked actin polymer networks to clusters with a scale-free size
distribution. This critical behavior occurs over an unexpectedly broad range of
crosslink concentrations. To understand this robustness, we develop a
quantitative model of contractile networks that takes into account network
restructuring: motors reduce connectivity by forcing crosslinks to unbind.
Paradoxically, to coordinate global contractions, motor activity should be low.
Otherwise, motors drive initially well-connected networks to a critical state
where ruptures form across the entire network.Comment: Main text: 21 pages, 5 figures. Supplementary Information: 13 pages,
8 figure
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