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Register a new userFluctuations of a membrane nanotube covered with an actin sleeve
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Many biological functions rely on the reshaping of cell membranes, in particular into nanotubes, which are covered in vivo by dynamic actin networks. Nanotubes are subject to thermal fluctuations, but the effect of these on cell functions is unknown. Here, we form nanotubes from liposomes using an optically trapped bead adhering to the liposome membrane. From the power spectral density of this bead, we study the nanotube fluctuations in the range of membrane tensions measured in vivo. We show that an actin sleeve covering the nanotube damps its high frequency fluctuations because of the network viscoelasticity. Our work paves the way for further studies on the effect of nanotube fluctuations in cellular functions.
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We study the force generation by a set of parallel actin filaments growing against an elastic membrane. The elastic membrane tries to stay flat and any deformation from this flat state, either caused by thermal fluctuations or due to protrusive polymerization force exerted by the filaments, costs energy. We study two lattice models to describe the membrane dynamics. In one case, the energy cost is assumed to be proportional to the absolute magnitude of the height gradient (gradient model) and in the other case it is proportional to the square of the height gradient (Gaussian model). For the gradient model we find that the membrane velocity is a non-monotonic function of the elastic constant $mu$, and reaches a peak at $mu=mu^ast$. For $mu < mu^ast$ the system fails to reach a steady state and the membrane energy keeps increasing with time. For the Gaussian model, the system always reaches a steady state and the membrane velocity decreases monotonically with the elastic constant $ u$ for all nonzero values of $ u$. Multiple filaments give rise to protrusions at different regions of the membrane and the elasticity of the membrane induces an effective attraction between the two protrusions in the Gaussian model which causes the protrusions to merge and a single wide protrusion is present in the system. In both the models, the relative time-scale between the membrane and filament dynamics plays an important role in deciding whether the shape of elasticity-velocity curve is concave or convex. Our numerical simulations agree reasonably well with our analytical calculations.
A broad range of membrane proteins display anomalous diffusion on the cell surface. Different methods provide evidence for obstructed subdiffusion and diffusion on a fractal space, but the underlying structure inducing anomalous diffusion has never been visualized due to experimental challenges. We addressed this problem by imaging the cortical actin at high resolution while simultaneously tracking individual membrane proteins in live mammalian cells. Our data confirm that actin introduces barriers leading to compartmentalization of the plasma membrane and that membrane proteins are transiently confined within actin fences. Furthermore, superresolution imaging shows that the cortical actin is organized into a self-similar meshwork. These results present a hierarchical nanoscale picture of the plasma membrane.
We present a simple approximate analytical estimate for self-energy of a charge in the middle of cylindrical channel of a high permittivity epsilon_1 in a media of a low permittivity epsilon_2 (for the cases of infinitely long and comparatively short channels) and show that this estimate is in a good quantitative agreement with exact solution of Poisson equation. Further, using these estimates, we explain the observed a lower conductivity, caused by an increased the self-free-energy for ions, whose diameter is by ~1 angstrom less than that of the channel (as compared to ions, whose diameter is equal to that of the channel).
The phase transition from the isotropic (I) to nematic (N) liquid crystalline suspension of F-actin of average length $3~mu$m or above was studied by local measurements of optical birefringence and protein concentration. Both parameters were detected to be continuous in the transition region, suggesting that the I-N transition is higher than 1st order. This finding is consistent with a recent theory by Lammert, Rokhsar & Toner (PRL, 1993, 70:1650), predicting that the I-N transition may become continuous due to suppression of disclinations. Indeed, few line defects occur in the aligned phase of F-actin. Individual filaments in solutions of a few mg/ml F-actin undergo fast translational diffusion along the filament axis, whereas both lateral and rotational diffusions are suppressed.
Amoeboid cell migration is characterized by frequent changes of the direction of motion and resembles a persistent random walk on long time scales. Although it is well known that cell migration is typically driven by the actin cytoskeleton, the cause of this migratory behavior remains poorly understood. We analyze the spontaneous dynamics of actin assembly due to nucleation promoting factors, where actin filaments lead to an inactivation of the nucleators. We show that this system exhibits excitable dynamics and can spontaneously generate waves, which we analyse in detail. By using a phase-field approach, we show that these waves can generate cellular random walks. We explore how the characteristics of these persistent random walks depend on the parameters governing the actin-nucleator dynamics. In particular, we find that the effective diffusion constant and the persistence time depend strongly on the speed of filament assembly and the rate of nucleator inactivation. Our findings point to a deterministic origin of the random walk behavior and suggest that cells could adapt their migration pattern by modifying the pool of available actin.
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