Invade to evade: E. coli's gutsy survival strategies.

Antibiotic resistance is often studied in vitro, limiting the understanding of in vivo mechanisms that affect antibiotic treatment. In this issue of Cell Host & Microbe, Rodrigues et al. show that specific mutations allow bacteria to invade intestinal cells in a mouse model, thereby evading antibiotic treatment.

Weak catch bonds make strong networks.

Molecular catch bonds are ubiquitous in biology and essential for processes like leucocyte extravasion and cellular mechanosensing. Unlike normal (slip) bonds, catch bonds strengthen under tension. The current paradigm is that this feature provides 'strength on demand', thus enabling cells to increase rigidity under stress.

Origin of Slow Stress Relaxation in the Cytoskeleton.

Dynamically cross-linked semiflexible biopolymers such as the actin cytoskeleton govern the mechanical behavior of living cells. Semiflexible biopolymers nonlinearly stiffen in response to mechanical loads, whereas the cross-linker dynamics allow for stress relaxation over time. Here we show, through rheology and theoretical modeling, that the combined nonlinearity in time and stress leads to an unexpectedly slow stress relaxation, similar to the dynamics of disordered systems close to the glass transition.

Response of an actin network in vesicles under electric pulses.

We study the role of a biomimetic actin network during the application of electric pulses that induce electroporation or electropermeabilization, using giant unilamellar vesicles (GUVs) as a model system. The actin cortex, a subjacently attached interconnected network of actin filaments, regulates the shape and mechanical properties of the plasma membrane of mammalian cells, and is a major factor influencing the mechanical response of the cell to external physical cues. We demonstrate that the presence of an actin shell inhibits the formation of macropores in the electroporated GUVs.