The somatic Golgi acts as an asymmetric MTOC within Drosophila neurons, and this, together with the action Kinesin-2, helps maintain minus-end-out microtubule polarity with proximal dendrites.
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.
Cryo-electron microscopy reconstructions of two microtubule-bound transport kinesins at 7 Å resolution reveal how microtubule track binding stimulates ADP release, primes the active site for ATP binding and enables force generation.
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.
Kinesin-4 KIF21B promotes rapid reorientation of the microtubule network during formation of immunological synapse in T cells by acting as a pausing and catastrophe-inducing factor that keeps microtubules short.
T cell progenitor homing into the thymus requires kindlin-3 to stabilize their adhesion to vascular integrin ligands when blood flow velocities and shear rates increase during development.
Dynein bypasses obstacles on microtubules more efficiently than single kinesin, and kinesins overcome this limitation when transporting intracellular cargos in teams.