The actin cortex at a glance.

Precisely controlled cell deformations are key to cell migration, division and tissue morphogenesis, and have been implicated in cell differentiation during development, as well as cancer progression. In animal cells, shape changes are primarily driven by the cellular cortex, a thin actomyosin network that lies directly underneath the plasma membrane. Myosin-generated forces create tension in the cortical network, and gradients in tension lead to cellular deformations. Recent studies have provided important insight into the molecular control of cortical tension by progressively unveiling cortex composition and organization. In this Cell Science at a Glance article and the accompanying poster, we review our current understanding of cortex composition and architecture. We then discuss how the microscopic properties of the cortex control cortical tension. While many open questions remain, it is now clear that cortical tension can be modulated through both cortex composition and organization, providing multiple levels of regulation for this key cellular property during cell and tissue morphogenesis

Why is the change of the Johari-Goldstein β-relaxation time by densification in ultrastable glass minor?

Ultrastable glasses (USG) formed by vapor deposition are considerably denser. The onset temperature of devitrification, Ton, is significantly higher than Ton or Tg of ordinary glass (OG) formed by cooling, which implies an increase of the structural α-relaxation time by many orders of magnitude in USG compared to that in OG at the same temperature. However, for a special type of secondary relaxation having properties strongly connected to those of the α-relaxation, called the Johari-Goldstein β-relaxation, its relaxation time in USG is about an order of magnitude slower than that in OG and it has nearly the same activation energy, Eβ. The much smaller change in τβ and practically no change in Eβ by densification in USG are in stark contrast to the behavior of the α-relaxation. This cannot be explained by asserting that the Johari-Goldstein (JG) β-relaxation is insensitive to densification in USG, since the JG β-relaxation strength is significantly reduced in USG to such a level that it would require several thousands of years of aging for an OG to reach the same state, and therefore the JG β-relaxation does respond to densification in USG like the α-relaxation. Here, we provide an explanation based on two general properties established from the studies of glasses and liquids at elevated pressures and applied to USG. The increase in density of the glasses formed under high pressure can be even larger than that in USG. One property is the approximate invariance of the ratio τα(Ton)/τβ(Ton) to density change at constant τα(Ton), and the other is the same ργ/T-dependence of τβ in USG and OG where ρ is the density and γ is a material constant. These two properties are derived using the Coupling Model, giving a theoretical explanation of the phenomena. The explanation is also relevant for a full understanding of the experimental result that approximately the same surface diffusion coefficient is found in USG and OG with and without physical aging, and ultrathin films of a molecular glass-former

Focal Adhesion-Independent Cell Migration.

Cell migration is central to a multitude of physiological processes, including embryonic development, immune surveillance, and wound healing, and deregulated migration is key to cancer dissemination. Decades of investigations have uncovered many of the molecular and physical mechanisms underlying cell migration. Together with protrusion extension and cell body retraction, adhesion to the substrate via specific focal adhesion points has long been considered an essential step in cell migration. Although this is true for cells moving on two-dimensional substrates, recent studies have demonstrated that focal adhesions are not required for cells moving in three dimensions, in which confinement is sufficient to maintain a cell in contact with its substrate. Here, we review the investigations that have led to challenging the requirement of specific adhesions for migration, discuss the physical mechanisms proposed for cell body translocation during focal adhesion-independent migration, and highlight the remaining open questions for the future

Why is surface diffusion the same in ultrastable, ordinary, aged, and ultrathin molecular glasses?

Recently Fakhraai and coworkers measured surface diffusion in ultrastable glass produced by vapor deposition, ordinary glass with and without physical aging, and ultrathin films of the same molecular glassformer, N,N0-bis(3-methylphenyl)-N,N0-diphenylbenzidine (TPD). Diffusion on the surfaces of all these glasses is greatly enhanced compared with the bulk diffusion similar to that previously found by others, but remarkably the surface diffusion coefficients DS measured are practically the same. The observed independence of DS from changes of structural a-relaxation due to densification or finite-size effect has an impact on the current understanding of the physical origin of enhanced surface diffusion. We have demonstrated before and also here that the primitive relaxation time t0 of the coupling model, or its analogue tb, the Johari–Goldstein b-relaxation, can explain quantitatively the enhancement found in ordinary glasses. In this paper, we assemble together considerable experimental evidence to show that the changes in tb and t0 of ultrastable glasses, aged ordinary glasses, and ultrathin-films are all insignificant when compared with ordinary glasses. Thus, in the context of the explanation of the enhanced surface diffusion given by the coupling model, these collective experimental facts on tb and t0 further explain approximately the same DS in the different glasses of TPD as found by Fakhraai and coworkers