New paradigm for glassy-like anomalies in solids from fundamental symmetries

Glasses and disordered materials are known to display anomalous features in the density of states, in the specific heat and in thermal transport. Nevertheless, in recent years, the question whether these properties are really anomalous (and peculiar of disordered systems) or rather more universal than previously thought, has emerged. New experimental and theoretical observations have questioned the origin of the boson peak (BP) and the linear in T specific heat exclusively from disorder and two-level systems (TLS). The same properties have been indeed observed in ordered or minimally disordered compounds and in incommensurate structures for which the standard explanations are not applicable. Using the formal analogy between phason modes (e.g., in quasicrystals and incommensurate lattices) and diffusions, and between amplitude modes and optical phonons, we suggest the existence of a more universal physics behind these properties. In particular, we strengthen the idea that linear in T specific heat is linked to low energy diffusive modes resulting from fundamental symmetries, and that a BP excess can be induced in crystals either by gapped optical-like modes and/or by anharmonic diffusive (Akhiezer) damping.

Wave simulation in double-porosity media based on the Biot-Rayleigh theory

We have developed a numerical algorithm for simulation of wave propagation in double-porosity media, where the pore space is saturated with a single fluid. Spherical inclusions embedded in a background medium oscillate to yield attenuation by mode conversion from fast P-wave energy to slow P-wave energy (mesoscopic or wave-induced fluid-flow loss). The theory is based on the Biot theory of poroelasticity and the Rayleigh model of bubble oscillations. The differential equation of the Biot-Rayleigh variable is approximated with the Zener mechanical model, which results in a memory-variable viscoelastic equation. These approximations are required to model mesoscopic losses arising from conversion of the fast P-wave energy to slow diffusive modes. The model predicts a relaxation peak in the seismic band, depending on the diameter of the patches, to model the attenuation level observed in rocks. The wavefield is obtained with a grid method based on the Fourier differential operator and a second-order time-integration algorithm. Because the presence of two slow quasistatic modes makes the differential equations stiff, a time-splitting integration algorithm is used to solve the stiff part analytically. The modeling has spectral accuracy in the calculation of the spatial derivatives.

Conformational states control Lck switching between free and confined diffusion modes in T cells

T cell receptor (TCR) phosphorylation by Lck is an essential step in T cell activation. It is known the conformational states of Lck control enzymatic activity; however, the underlying principles of how Lck finds its substrate in the plasma membrane remain elusive. Here, single-particle tracking is paired with photoactivatable localization microscopy (sptPALM) to observe the diffusive modes of Lck in the plasma membrane. Individual Lck molecules switched between free and confined diffusion in resting and stimulated T cells. Conformational state, but not partitioning into membrane domains, caused Lck confinement as open conformation Lck was more confined than closed. Further confinement of kinase-dead versions of Lck suggests that Lck interacts with open active Lck to cause confinement, irrespectively of kinase activity. Our data supports a model that confined diffusion of open Lck results in high local phosphorylation rates and closed Lck diffuses freely to enable wide-range scanning of the plasma membrane.

Biased Brownian motion as a mechanism to facilitate nanometer-scale exploration of the microtubule plus end by a kinesin-8

Kinesin-8s are plus-end–directed motors that negatively regulate microtubule (MT) length. Well-characterized members of this subfamily (Kip3, Kif18A) exhibit two important properties: (i) They are “ultraprocessive,” a feature enabled by a second MT-binding site that tethers the motors to a MT track, and (ii) they dissociate infrequently from the plus end. Together, these characteristics combined with their plus-end motility cause Kip3 and Kif18A to enrich preferentially at the plus ends of long MTs, promoting MT catastrophes or pausing. Kif18B, an understudied human kinesin-8, also limits MT growth during mitosis. In contrast to Kif18A and Kip3, localization of Kif18B to plus ends relies on binding to the plus-end tracking protein EB1, making the relationship between its potential plus-end–directed motility and plus-end accumulation unclear. Using single-molecule assays, we show that Kif18B is only modestly processive and that the motor switches frequently between directed and diffusive modes of motility. Diffusion is promoted by the tail domain, which also contains a second MT-binding site that decreases the off rate of the motor from the MT lattice. In cells, Kif18B concentrates at the extreme tip of a subset of MTs, superseding EB1. Our data demonstrate that kinesin-8 motors use diverse design principles to target MT plus ends, which likely target them to the plus ends of distinct MT subpopulations in the mitotic spindle.