Novel steady state of a microtubule assembly in a confined geometry

We study the steady state of an assembly of microtubules in a confined volume, analogous to the situation inside a cell where the cell boundary forms a natural barrier to growth. We show that the dynamical equations for growing and shrinking microtubules predict the existence of two steady states, with either exponentially decaying or exponentially increasing distribution of microtubule lengths. We identify the regimes in parameter space corresponding to these steady states. In the latter case, the apparent catastrophe frequency near the boundary was found to be significantly larger than that in the interior. Both the exponential distribution of lengths and the increase in the catastrophe frequency near the cell margin is in excellent agreement with recent experimental observations.Comment: 8 pages, submitted to Phys. Rev.

Transport enhancement from incoherent coupling between one-dimensional quantum conductors

We study the non-equilibrium transport properties of a highly anisotropic two-dimensional lattice of spin-1/2 particles governed by a Heisenberg XXZ Hamiltonian. The anisotropy of the lattice allows us to approximate the system at finite temperature as an array of incoherently coupled one-dimensional chains. We show that in the regime of strong intrachain interactions, the weak interchain coupling considerably boosts spin transport in the driven system. Interestingly, we show that this enhancement increases with the length of the chains, which is related to superdiffusive spin transport. We describe the mechanism behind this effect, compare it to a similar phenomenon in single chains induced by dephasing, and explain why the former is much stronger

Weak measurement takes a simple form for cumulants

A weak measurement on a system is made by coupling a pointer weakly to the system and then measuring the position of the pointer. If the initial wavefunction for the pointer is real, the mean displacement of the pointer is proportional to the so-called weak value of the observable being measured. This gives an intuitively direct way of understanding weak measurement. However, if the initial pointer wavefunction takes complex values, the relationship between pointer displacement and weak value is not quite so simple, as pointed out recently by R. Jozsa. This is even more striking in the case of sequential weak measurements. These are carried out by coupling several pointers at different stages of evolution of the system, and the relationship between the products of the measured pointer positions and the sequential weak values can become extremely complicated for an arbitrary initial pointer wavefunction. Surprisingly, all this complication vanishes when one calculates the cumulants of pointer positions. These are directly proportional to the cumulants of sequential weak values. This suggests that cumulants have a fundamental physical significance for weak measurement

Actin disassembly by cofilin, coronin, and Aip1 occurs in bursts and is inhibited by barbed-end cappers

Turnover of actin filaments in cells requires rapid actin disassembly in a cytoplasmic environment that thermodynamically favors assembly because of high concentrations of polymerizable monomers. We here image the disassembly of single actin filaments by cofilin, coronin, and actin-interacting protein 1, a purified protein system that reconstitutes rapid, monomer-insensitive disassembly (Brieher, W.M., H.Y. Kueh, B.A. Ballif, and T.J. Mitchison. 2006. J. Cell Biol. 175:315–324). In this three-component system, filaments disassemble in abrupt bursts that initiate preferentially, but not exclusively, from both filament ends. Bursting disassembly generates unstable reaction intermediates with lowered affinity for CapZ at barbed ends. CapZ and cytochalasin D (CytoD), a barbed-end capping drug, strongly inhibit bursting disassembly. CytoD also inhibits actin disassembly in mammalian cells, whereas latrunculin B, a monomer sequestering drug, does not. We propose that bursts of disassembly arise from cooperative separation of the two filament strands near an end. The differential effects of drugs in cells argue for physiological relevance of this new disassembly pathway and potentially explain discordant results previously found with these drugs

Motile cilia defects in diseases other than primary ciliary dyskinesia:The contemporary diagnostic and research role for transmission electron microscopy

Ultrastructural studies have underpinned the cell biological and clinical investigations of the varied roles of motile cilia in health and disease, with a long history since the 1950s. Recent developments from transmission electron microscopy (TEM; cryo-electron microscopy, electron tomography) have yielded higher resolution and fresh insights into the structure and function of these complex organelles. Microscopy in ciliated organisms, disease models, and in patients with ciliopathy diseases has dramatically expanded our understanding of the ubiquity, multisystem involvement, and importance of cilia in normal human development. Here, we review the importance of motile cilia ultrastructural studies in understanding the basis of diseases other than primary ciliary dyskinesia

An Explicit Bound for Dynamical Localisation in an Interacting Many-Body System

We characterise and study dynamical localisation of a finite interacting quantum many-body system. We present explicit bounds on the disorder strength required for the onset of localisation of the dynamics of arbitrary ensemble of sites of the XYZ spin-1/2 model. We obtain these results using a novel form of the fractional moment criterion, which we establish, together with a generalisation of the self-avoiding walk representation of the system Green's functions, called path-sums. These techniques are not specific to the XYZ model and hold in a much more general setting. We further present bounds for two observable quantities in the localised regime: the magnetisation of any sublattice of the system as well as the linear magnetic response function of the system. We confirm our results through numerical simulations.Comment: 35 pages; 5 figure

Quantitative predictions on auxin-induced polar distribution of PIN proteins during vein formation in leaves

The dynamic patterning of the plant hormone auxin and its efflux facilitator the PIN protein are the key regulator for the spatial and temporal organization of plant development. In particular auxin induces the polar localization of its own efflux facilitator. Due to this positive feedback auxin flow is directed and patterns of auxin and PIN arise. During the earliest stage of vein initiation in leaves auxin accumulates in a single cell in a rim of epidermal cells from which it flows into the ground meristem tissue of the leaf blade. There the localized auxin supply yields the successive polarization of PIN distribution along a strand of cells. We model the auxin and PIN dynamics within cells with a minimal canalization model. Solving the model analytically we uncover an excitable polarization front that triggers a polar distribution of PIN proteins in cells. As polarization fronts may extend to opposing directions from their initiation site we suggest a possible resolution to the puzzling occurrence of bipolar cells, such we offer an explanation for the development of closed, looped veins. Employing non-linear analysis we identify the role of the contributing microscopic processes during polarization. Furthermore, we deduce quantitative predictions on polarization fronts establishing a route to determine the up to now largely unknown kinetic rates of auxin and PIN dynamics.Comment: 9 pages, 4 figures, supplemental information included, accepted for publication in Eur. Phys. J.