Axon repulsion in response to the midline repellent slit depends on an evolutionary conserved interaction between the Roundabout receptor and the wave regulatory complex.

The cryo-electron microscopy structure of an assembly of the WAVE Regulatory Complex and its activator, the Rac GTPase, plus complementary biochemistry and biophysics, reveal a novel activation mechanism involving two distinct Rac binding sites.

Neurexin–Neuroligin1 complex positively regulates F-actin assembly through direct interaction with WAVE complex to control normal synaptic growth and electrophysiological function in Drosophila neuromuscular junction.

An unbiased biochemical screen reveals a direct link between gene regulation and actin cytoskeleton remodeling.

Fat2 signals from the trailing edge of each cell to localize WAVE activity to the leading edge of the cell behind, polarizing protrusive regions within cells and across the epithelium.

By moving from correlations to causality in cancer signal transduction using optogenetics, the sufficiency of RalB activation to trigger invasion and the underlying molecular mechanisms were established.

The dendrite branching receptor HPO-30 modulates actin dynamics by binding to both WAVE complex and actin filaments.

Transferrin receptor 1-mediated iron uptake plays a pivotal role in osteoclast energy metabolism and cytoskeleton and regulates bone remodeling in female mice.

Propagation, speed and shapes of genetic waves of expression during development can be modeled by a simple interplay between two transcriptional modules (dynamic/static), which explains robustness and precision of patterning.

Cell stretch release generates plasma membrane (PM) evaginations of ≈100 nm, triggering a local event of actin polymerization that flattens and recovers PM shape.