The dynamin GTPase mediates regenerative axonal fusion in by regulating fusogen levels.

Axonal fusion is a neuronal repair mechanism that results in the reconnection of severed axon fragments, leading to the restoration of cytoplasmic continuity and neuronal function. While synaptic vesicle recycling has been linked to axonal regeneration, its role in axonal fusion remains unknown. Dynamin proteins are large GTPases that hydrolyze lipid-binding membranes to carry out clathrin-mediated synaptic vesicle recycling.

Novel putative interactors of FZO-1/mitofusin 2 identified using large-scale yeast two-hybrid screening in .

Mitochondria are energy-converting organelles that shift between fusion and fission states in order to perform a variety of essential functions. Disruption of these dynamics is detrimental to cellular health and is associated with a range of human diseases. Mitofusin 2 is an essential large GTPase protein that orchestrates fusion of outer mitochondria membranes, and mutations in the encoding gene are causative for Charcot-Marie-Tooth disease.

Mutation of the H12-helix of α-tubulin/MEC-12 disrupts the localization of neuronal mitochondria.

Microtubules are essential components of the cytoskeleton that allow bi-lateral neuronal transport. Correct regulation of these complex intracellular transport processes is central to neuronal function. However, despite major advancements in our knowledge, we still lack a complete understanding on how neuronal transport is regulated.

Synaptic branch stability is mediated by non-enzymatic functions of MEC-17/αTAT1 and ATAT-2.

Microtubules are fundamental elements of neuronal structure and function. They are dynamic structures formed from protofilament chains of α- and β-tubulin heterodimers. Acetylation of the lysine 40 (K40) residue of α-tubulin protects microtubules from mechanical stresses by imparting structural elasticity.

DYN-1/dynamin regulates microtubule dynamics after axon injury.

Microtubules play essential roles in the regeneration of axons after injury, but precisely how their growth is regulated remains to be resolved. Here, we studied the influence of the DYN-1/dynamin GTPase protein on microtubule growth after axon injury. Before injury, loss of DYN-1 had no effect on microtubule dynamics compared to wild-type animals.