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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.
Yang, Golkaram et al. reported that in human embryonic stem cells, cellular crowding leads to the blockade of FGFR1 endocytosis, resulting in a decrease in ETV4 expression. This, in turn, derepresses the neuroectoderm fate.
Using micropipette aspiration on donated human embryos, cell surface tensions during compaction were mapped, indicating a role for defective cell contractility in poor quality embryos.
When studying nematic ordering of cells in a monolayer, it is commonly assumed that the principal stress and cell shape axes are tightly coupled. Here, the authors measure cell shape and cell-generated contractile stresses and show that cells in monolayers form correlated, dynamic domains in which the stresses are systematically misaligned with the cell bodies.
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.