a b s t r a c tWe investigate how the crossover temperature of the elastic-plastic transition, the 'vitrification point' T v , changes under load for isotropic vitrimers and exchangeable liquid crystal elastomers (xLCEs), using the thermoplastic SIS triblock polymer as a reference. In all these cases, the elastic network cross-links are transient: physical micro-phase separation in SIS and covalent transesterification bonds in vitrimers. From the analysis of SIS we define T v as the point when entropic rubber-elasticity contraction due to heating under load turns into the irreversible plastic extension due to cross-links breaking and reforming. In xLCEs, the response to mechanical stress is heavily influenced by the smectic liquidcrystalline order, which makes the material much stiffer than normal rubbery networks, and also leads to the shape-memory effect across the smectic-isotropic transition point. The vitrification in the isotropic phase of xLCE, and in isotropic vitrimers, was found to be independent of stress, which can be attributed to the thermal activity of the catalyst determining T v and it not being mechanically coupled to the elastic network. Beyond T v , with increasing stress the plastic extension rapidly increases with temperature, as cross-link dynamics becomes more apparent.

When plated onto substrates, cell morphology and even stem cell differentiation are influenced by the stiffness of their environment. Stiffer substrates give strongly spread (eventually polarized) cells with strong focal adhesions, and stress fibers; very soft substrates give a less developed cytoskeleton, and much lower cell spreading. The kinetics of this process of cell spreading is studied extensively, and important universal relationships are established on how the cell area grows with time. Here we study the population dynamics of spreading cells, investigating the characteristic processes involved in cell response to the substrate. We show that unlike the individual cell morphology, this population dynamics does not depend on the substrate stiffness. Instead, a strong activation temperature dependence is observed. Different cell lines on different substrates all have long-time statistics controlled by the thermal activation over a single energy barrier ∆G ≈ 19 kcal/mol, while the early-time kinetics follows a power law ∼ t 5 . This implies that the rate of spreading depends on an internal process of adhesion complex assembly and activation: the operational complex must have 5 component proteins, and the last process in the sequence (which we believe is the activation of focal adhesion kinase) is controlled by the binding energy ∆G.

No abstract

When plated onto substrates, cell morphology and even stem cell differentiation are influenced by the stiffness of their environment. Stiffer substrates give strongly spread (eventually polarized) cells with strong focal adhesions, and stress fibers; very soft substrates give a less developed cytoskeleton, and much lower cell spreading. The kinetics of this process of cell spreading is studied extensively, and important universal relationships are established on how the cell area grows with time.Here we study the population dynamics of spreading cells, investigating the characteristic processes involved in cell response to the substrate. We show that unlike the individual cell morphology, this population dynamics does not depend on the substrate stiffness. Instead, a strong activation temperature dependence is observed. Different cell lines on different substrates all have long-time statistics controlled by the thermal activation over a single energy barrier ∆G ≈ 19 kcal/mol, while the early-time kinetics follows a power law ∼ t 5 . This implies that the rate of spreading depends on an internal process of adhesion-mechanosensing complex assembly and activation: the operational complex must have 5 component proteins, and the last process in the sequence (which we believe is the activation of focal adhesion kinase) is controlled by the binding energy ∆G.

No abstract