Stress fibres articles from across Nature Portfolio

Actomyosin networks constrict cell area and junctions to alter cell and tissue shape. Here, Li et al. reveal a morphological cell expansion wave behaviour that coordinates epithelial flattening and tissue elongation during Drosophila oogenesis.

ZNF185 is identified as a novel PKA substrate and found to be important for the organization of endothelial cell–cell junctions and suppression of vascular hyperpermeability by regulating the cAMP/PKA/RhoA signaling pathway.

Matrix stiffening is a quintessential feature of aged tissues. Authors show that an aged (stiff) matrix epigenetically represses the gene encoding the longevity factor, α-Klotho, resulting in chondrocyte dysfunction, a leading cause of osteoarthritis.

The TAM family of receptor tyrosine kinases exerts pleiotropic functions in health and disease. Here, the authors show that TAM receptors control osteoblastic bone formation and identified MERTK as a novel target for bone anabolic therapy and mitigation of bone metastasis including its associated osteolytic bone disease

In this study the authors report that Caldesmon controls force-balance and architecture of stress fibers through dynamic cross-linking of actin and myosin filaments. Caldesmon depletion led to consequent problems in cell morphogenesis, motility and mechanosensing.

Stress fibres form a fully integrated meshwork with the submembranous contractile actin cortex that generates and propagates traction forces across the entire cell.

In cells exposed to stiff extracellular matrix, sequestration of the ubiquitin ligase TRIM21 by actin stress fibres can prevent the ubiquitination and breakdown of the glycolytic enzyme PFK, directly linking mechanical sensing to metabolic regulation.