Boraas et al. identify that mRNAs and the stress granule RNA-binding protein G3BP1 form ribonucleoprotein (RNP) complexes at FAs. These RNPs regulate FA protein mobility and cell migration under norma...

Integrin-adhesion complexes (IACs) form spontaneously in cells on extracellular matrix substrates, allowing them to sense matrix composition and transduce force. However, IACs often do not form unifor...

Congenital vascular malformations result from abnormal development of the vascular tree, with the aneurysmal malformation of the vein of Galen (VGAM) being the most prevalent neurovascular malformation in neonates, associated with poor outcomes. This condition is linked to germline mutations in the RASA1 and EPHB4 genes, although the underlying developmental mechanisms remain unclear. Here we generate zebrafish models lacking rasa1a and ephb4a that replicate the genetic and structural features of VGAMs. Our findings connect the development of malformations to insufficient fusion of precursor blood vessels, a process regulated by blood flow and the responses of endothelial cells. RASA1 deficiency destabilizes the homeostatic response to blood flow and contributes to impaired flow-mediated activation of MAPK and phosphatidylinositol-3-kinase signaling. By pharmacologically targeting these signaling pathways in mutant models, we restore normal fusion in existing malformations, offering po

Bone marrow health is central to transplantations, blood formation, and cancer progression. However, the bone marrow niche deteriorates with age, impairing haematopoietic stem cell function. Contrary ...

Researchers show that embryonic skin stem cells rely on a specialized mechanism to resist injury. The findings could lead to new strategies for repairing wounds

Researchers are testing multiple treatments for the rare genetic conditions

RAEFISH delivers whole-transcriptome (>20,000 genes) imaging at single-molecule resolution in cells and tissues and enables direct gRNA detection for high-content, image-based CRISPR screens.

Traction force and FAK signaling exhibit oscillatory temporal coupling in adhesive structures.

Embryo growth, morphogenesis, and patterning are complex processes that coordinate between cellular dynamics, fate specification, and multiscale physical forces. Understanding how robustness in embryo development is achieved despite inherent heterogeneities in gene expression, cell properties, and tissue growth is a fundamental question. Although various feedback between gene expression, signaling, and cell and tissue mechanics have been uncovered to confer robustness on developmental systems, measuring variability and robustness from a quantitative perspective often remains challenging. Furthermore, cell fate plasticity, a key mechanism that can confer robustness, is lacking in many developing tissues. This review highlights how recent technological and conceptual advances in quantitative approaches to biology help to overcome these bottlenecks, with a particular focus on how mechanochemical feedback, or alternatively, selectively tuned control parameters, ensure developmental robustness.

The authors discover a homeostatic process termed interstasis, in which an increased concentration of proteins within RNA–protein condensates induces the sequestration of their own mRNAs.

McCreery, Stubb et al. show that mechano-osmotic changes in the nucleus induce general transcriptional repression and prime chromatin for cell fate transitions by relieving repression of specific differentiation genes.