Studies of Lowe syndrome patient cells, which lack the inositol 5-phosphatase OCRL, suggest that a defect in endocytosis plays a role in the pathological manifestations of the disease.

Profilin helps to maintain formin at the growing barbed end of an actin filament, while piconewton mechanical tension drastically enhances formin dissociation from the barbed end.

Microtubules orchestrate wound repair and innate immune response in the Caenorhabditis elegans epidermis.

Experiments using purified proteins reveal how the network of filaments that underlie cell movement becomes denser when pushing against a stronger mechanical force.

Cortical dynein organizes unipolar microtubule arrays in Drosophila axons by expelling minus-end-out microtubules.

Intersectin counterparts in yeast recruit WASP and WIP to endocytic sites to establish a robust multivalent SH3 domain-PRM interaction network which gives actin assembly onset a switch-like behavior in vivo.

Cryo-EM structures of actomyosin VI in multiple nucleotide states reveal a unique actin-myosin interface and a mechanism of force-sensitivity; furthermore, myosin VI remodels F-actin, suggesting a role for actin structural plasticity during force generation.

Teneurin-2, a synaptic organizer, localizes to microtubule-rich inhibitory synapses and recruits microtubules via interaction with end-binding proteins, and this mechanism enables GABA_A receptors exocytosis.

Sarcomeres in heart muscle cells come from stress fiber-like structures that are mechanistically distinct from stress fibers in non-muscle cells.

Biophysical and structural studies reveal how low piconewton forces across actin enhance binding by the critical cell-cell adhesion protein α-catenin versus its force insensitive homolog vinculin.