Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Mechanotransduction refers to the processes through which cells sense and respond to mechanical stimuli by converting them to biochemical signals that elicit specific cellular responses.
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.
During alveologenesis myofibroblasts contractions at terminal sacs produce alveoli in the lungs. Here they show that endothelial cells promote myofibroblast-driven alveologenesis by forming basement membranes via Rap1-induced integrin β1 activation.
Cells exert tight control over the size of their compartments in order to regulate their function. Here, nuclear fluorescence exclusion microscopy is able to measure the nuclear and cytoplasmic volumes of live cells in a high-throughput way.
Extracellular matrix stiffness induces differential tension within integrinbased adhesions but it is not known if this is solely from myosin activity. Here, it is shown that 3T3 fibroblasts still transmit stiffness-dependent traction even with the absence of myosin contractility.
This study provides insights into the directional catch bonding of the linker protein vinculin by elucidating the molecular basis of mechanical reinforcement as well as unveiling its key role in subcellular organization and cellular processes.
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.
Extracellular matrix (ECM) stiffening is a hallmark of cancer aggressiveness. Diverse ECM environments can alter the number and cargo of small extracellular vesicles (sEVs). Wu et al. now delineate a pathway from ECM stiffness to FAK/PI3K/Akt signalling and Rab8-induced sEV secretion, promoting cancer growth.
The nuclear pore complex (NPC) regulates transport of macromolecules into and out of the nucleus. A study now shows that mechanical force applied on the nucleus affects the transport rates across the NPC diffusion barrier, modulating the nuclear localization of certain cargos.
Extracellular matrix (ECM) rigidity increases during tumour progression. In a recent study, Romani et al. delineated a connection between ECM stiffness and the redox response of disseminated tumour cells. Their results suggest that soft ECM promotes DRP1-mediated mitochondrial fission and an NRF2-dependent antioxidant response.