Synaptic defects previously attributed to loss of kinesin function are found to be mediated by the Wnd/DLK axonal injury signaling pathway, which restrains the total levels of presynaptic proteins in response to their accumulation.
Disrupting synapse formation between the retina and the brain in zebrafish larvae-by eliminating the molecular motor Kif5A-triggers a compensatory increase in the branching of retinal axons aimed at restoring synapse number.
Release site heterogeneity represents a previously unknown level of structural and functional organization within individual active zones in central synapses, which determines the spatiotemporal dynamics of multi-vesicular release.
The examination of the ultra-structure and in vivo dynamics of endocytosis in plants reveal plants unique actin-independent, clathrin-mediated endocytosis mechanisms to overcome their unique physiological properties.
Biochemical, single molecule, cell and structural biology studies reveal an interaction between the kinesin-5 tail and motor domains regulating high-force production, which is critical for microtubule sliding motility.