Cadherins articles from across Nature Portfolio

Schliffka et al. show that in the early mouse embryo, hemispherical intrusions, or inverse blebs, grow into cells at cell–cell adhesion sites in response to luminal fluid accumulation and pressure build-up, and may serve as pumps moving fluid into hydraulic sinks.

An endothelial mechanobiology study on the role of hydrostatic pressure suggests that values mimicking microvascular pressure promote sprouting angiogenesis through the activation of YAP signaling.

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.

By using a CRISPR/dCas9 biosensor that reads DNA methylation of α-satellite repeats in live cells, we identify a signaling pathway linking the chromatin and transcriptional state of repeats to the integrity of epithelial adherens junctions.

The authors identified a cell population in Drosophila follicles that elaborate filopodia penetrating the oocyte they are contacting. These somatic cells are essential during oogenesis to regulate polarity and germline development of the future embryo.

The presence of CD8⁺ T cells in the cytoplasm of biliary epithelial cells (BEC) has been associated with primary biliary cholangitis. Here, the authors demonstrate that CD8⁺ T cells invade BEC using a mechanism that is dependent on cytoskeletal rearrangements and E-cadherin:β-catenin interactions.

Loss of VEGF-C or VEGFR3 function or gain of VE-cadherin function causes identical defects in sinusoidal and lymphatic growth, resulting in anemia and lymphedema. Mechanistically, VEGF-C drives VE-cadherin phosphorylation and endocytosis whereas VE-cadherin prevents VEGFR3 internalization and downstream growth factor signaling. In the absence of VEGFR3, reducing VE-cadherin levels rescues vascular growth by potentiating VEGF-C–VEGFR2 signaling.

Epithelial cells form energetically costly cell–cell adhesions in response to mechanical forces. How cells obtain their energy during this event is unclear. Activity of a key regulator of cell metabolism, the AMP-activated protein kinase (AMPK), is now shown to be mechanoresponsive, and thus can bridge adhesion mechanotransduction and energy homeostasis.

Tumours are highly complex and contain multiple cell types. Cancer-associated fibroblasts are now shown to have a critical role in directly leading cancer cell invasion. This intercellular interaction relies on a mechanically active cadherin-based junction, and CAF-led invasion is demonstrated to require E-cadherin in the cancer cell.

Cadherin adhesion complexes have recently emerged as sensors of tissue tension that regulate key developmental processes. Super-resolution microscopy experiments now unravel the spatial organization of the interface between cadherins and the actin cytoskeleton and reveal how vinculin, a central component in cadherin mechanotransduction, is regulated by mechanical and biochemical signals.

Many cell types in our body move in a collective manner, which requires individual cells to align their movements relative to that of their neighbours. A mechanism is now described in which cadherin-rich protrusions are extended from leading migrating cells and engulfed by follower cells to guide collective migration.