Spontaneous flow created by active topological defects.

Topological defects are at the root of the large-scale organization of liquid crystals. In two-dimensional active nematics, two classes of topological defects of charges [Formula: see text] are known to play a major role due to active stresses. Despite this importance, few analytical results have been obtained on the flow-field and active-stress patterns around active topological defects. Using the generic hydrodynamic theory of active systems, we investigate the flow and stress patterns around these topological defects in unbounded, two-dimensional active nematics. Under generic assumptions, we derive analytically the spontaneous velocity and stall force of self-advected defects in the presence of both shear and rotational viscosities. Applying our formalism to the dynamics of monolayers of elongated cells at confluence, we show that the non-conservation of cell number generically increases the self-advection velocity and could provide an explanation for their observed role in cellular extrusion and multilayering. We finally investigate numerically the influence of the Ericksen stress. Our work paves the way to a generic study of the role of topological defects in active nematics, and in particular in monolayers of elongated cells.

Observation of rapid exciton-exciton annihilation in monolayer molybdenum disulfide.

Monolayer MoS2 is a direct-gap two-dimensional semiconductor that exhibits strong electron-hole interactions, leading to the formation of stable excitons and trions. Here we report the existence of efficient exciton-exciton annihilation, a four-body interaction, in this material. Exciton-exciton annihilation was identified experimentally in ultrafast transient absorption measurements through the emergence of a decay channel varying quadratically with exciton density. The rate of exciton-exciton annihilation was determined to be (4.3 ± 1.1) × 10(-2) cm(2)/s at room temperature.

Mechanically-driven growth and competition in a Voronoi model of tissues.

The mechanisms leading cells to acquire a fitness advantage and establish themselves in a population are paramount to understanding the development and growth of cancer. Although there are many works that study separately either the evolutionary dynamics or the mechanics of cancer, little has been done to couple evolutionary dynamics to mechanics. To address this question, we study a confluent model of tissue using a Self-Propelled Voronoi (SPV) model with stochastic growth rates that depend on the mechanical variables of the system. The SPV model is an out-of-equilibrium model of tissue derived from an energy functional that has a jamming/unjamming transition between solid-like and liquid-like states. By considering several scenarios of mutants invading a resident population in both phases, we determine the range of parameters that confer a fitness advantage and show that the preferred area and perimeter are the most relevant ones. We find that the liquid-like state is more resistant to invasion and show that the outcome of the competition can be determined from the simulation of a non-growing mixture. Moreover, a mean-field approximation can accurately predict the fate of a mutation affecting mechanical properties of a cell. Our results can be used to infer evolutionary dynamics from tissue images, understand cancer-suppressing effects of tissue mechanics, and even search for mechanics-based therapies.

Crisscross multilayering of cell sheets.

Hydrostatic skeletons such as the Hydra's consist of two stacked layers of muscle cells perpendicularly oriented. In vivo, these bilayers first assemble, and then the muscle fibers of both layers develop and organize with this crisscross orientation. In the present work, we identify an alternative mechanism of crisscross bilayering of myoblasts in vitro, which results from the prior local organization of these active cells in the initial monolayer. The myoblast sheet can be described as a contractile active nematic in which, as expected, most of the +1/2 topological defects associated with this nematic order self-propel. However, as a result of the production of extracellular matrix (ECM) by the cells, a subpopulation of these comet-like defects does not show any self-propulsion. Perpendicular bilayering occurs at these stationary defects. Cells located at the head of these defects converge toward their core where they accumulate until they start migrating on top of the tail of the first layer, while the tail cells migrate in the opposite direction under the head. Since the cells keep their initial orientations, the two stacked layers end up perpendicularly oriented. This concerted process leading to a crisscross bilayering is mediated by the secretion of ECM.