Abstract
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 because of 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.
Highlights
The plasma membrane is a complex fluid where lipids and proteins continuously interact and generate signaling platforms in order to communicate with the outside world
Voltage-gated potassium channels Kv1.4 and Kv2.1 were expressed in human embryonic kidney (HEK) cells, labeled with quantum dots (QDs) [15] and imaged using total internal reflection fluorescence (TIRF) microscopy at
Note that 41% is slightly above the percolation threshold. These results show that the motion of Kv channels in the plasma membrane is better modeled by percolation, i.e., obstructed diffusion, rather than motion in a viscoelastic medium, i.e., fractional Brownian motion (fBM)
Summary
The plasma membrane is a complex fluid where lipids and proteins continuously interact and generate signaling platforms in order to communicate with the outside world. One of the key mechanisms by which membrane molecules search reaction sites is based on lateral diffusion Quantitative imaging methods, such as single-particle tracking [1,2,3,4], spatiotemporal image correlation spectroscopy [5], fluorescence correlation spectroscopy (FCS) [6,7], and stimulated emission depletion (STED)-FCS [8,9], show that the dynamics of proteins and lipids in the plasma membrane often deviate from normal diffusion. The mean square displacement (MSD) does not grow linearly in time as expected for Brownian motion [10,11,12,13] This behavior suggests processes that hinder diffusion. Since the formation of protein complexes is governed by diffusion-mediated encounters, hindered diffusion plays fundamental roles in cell function
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