Vinculin-mediated axon growth requires interaction with actin but not talin in mouse neocortical neurons

The actin-binding protein vinculin is a major constituent of focal adhesion, but its role in neuronal development poorly understood. We found that deletion mouse neocortical neurons attenuated axon growth both vitro and vivo. Using functional mutants, we expression constitutively active significantly enhanced while the head-neck domain had an inhibitory effect. Interestingly, vinculin-talin interaction was dispensable for migration. Strikingly, tail delayed migration, increased branching, stunted axon. Inhibition Arp2/3 complex or abolishing with actin completely reversed branching phenotype caused by without affecting length. Super-resolution microscopy showed mobility expressing neurons. Our results provide novel insights into domains regulating migration growth.