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Cell adhesion is the process by which cells form contacts with each other or with their substratum through specialized protein complexes. Intercellular adhesion can be mediated by adherens junctions, tight junctions and desmosomes, whereas cells can interact with extracellular matrix molecules through focal adhesions.
Actomyosin and microtubule-based forces are both important for tissue development, but how these systems interact in space and time remains unclear. Here, the authors study fly wing epithelium growth and determine aspects driving cell shape that are driven by microtubule or actomyosin-generated forces.
Tissues undergo changes in their mechanical and material properties through alterations in cytoskeleton organization, extracellular matrix adhesion and cell–cell connectivity. These mechanical state transitions orchestrate cell proliferation and movement and tissue growth during development, in adult tissue repair and in disease contexts.
Catch bonds are unique protein-protein interactions where the bond lifetime increases under external pulling forces. Here, the authors engineer an artificial catch bond based on a non-catch bonding human gut bacterial adhesion protein complex.
In this Tools of the Trade article, Isomursu (Ivaska lab) describes a new method for dynamic micropatterning, which enables investigation of cell adhesion and migration on substrates that mimic different extracellular matrix environments.
Recently published in Nature, Fan et al. demonstrate that accumulation of advanced glycation end-products in the extracellular matrix of the liver increases viscoelasticity to promote hepatocellular carcinoma growth, independent of stiffness.
Cell–cell adhesions are inevitably exposed to mechanical forces. A landmark paper by Yonemura et al. identified how tension alters molecular function of the cadherin adhesion apparatus. Its legacy lies in the many on-going efforts to understand how mechanical force is used in cell–cell communication.
Effective pharmacological treatment options for abdominal aortic aneurysm (AAA) are missing. A study by Zhang et al. suggests that targeting the thrombo-inflammatory activity of platelets by blocking the intracellular accumulation of ceramides might limit AAA progression while not affecting hemostatic platelet function.
A new biotinylation-based approach identifies previously unknown cell surface proteins of the axonal initial segment (AIS) and shows a role for contactin-1 in assembly of the AIS extracellular matrix.