ATP-dependent microtubule severing protein that specifically recognizes and cuts microtubules (PubMed:17531954, PubMed:19619244, PubMed:22561316, PubMed:18202664). Probably by regulating microtubule remodeling, plays a role in new synapse formation in GABAergic DD (Dorsal D type) neurons (PubMed:26051896). n ATP + n H2O + a microtubule = n ADP + n phosphate + (n+1) alpha/beta tubulin heterodimers. Homohexamer (PubMed:19619244, PubMed:22561316). The homohexamer is stabilized by ATP-binding (By similarity). The homohexamer may adopt a ring conformation through which microtubules pass prior to being severed. Interacts with microtubules (By similarity). Interacts (via N-terminus) with tubulin; the interaction is direct (PubMed:19619244). Forms an intramembrane hairpin-like structure in the membrane (By similarity). Localizes to the cytoskeleton, perinuclear region and cytoplasm in early embryos (PubMed:17531954). Expressed at all developmental stages (PubMed:17531954). Highly expressed in the embryo and expressed at lower levels in L3-L4 larvae (PubMed:17531954). Highly expressed in the embryo (PubMed:17531954). Not expressed in L3-L4 larvae (PubMed:17531954). The MTBD (microtubule binding domain) region mediates binding to microtubules and tubulin. Slow growth, reduced brood size, abnormal oogenesis and multiple vulvae (PubMed:17531954). Progressive locomotor defects, which is rescued following exposure to the drugs guanabenz, salubrinal, phenazine, or methylene blue (PubMed:26744324). Lifespan is prolonged following exposure to the drugs guanabenz, salubrinal or methylene blue, but not phenazine (PubMed:26744324). Increases numbers of centrosomal microtubules in early embryos (PubMed:17531954). Reduced neutral lipid levels in intestinal cells (PubMed:25875445). RNAi-mediated knockdown results in paralysis due to an increase in the endoplasmic reticulum stress response, which is rescued following exposure to the drugs methylene blue, guanabenz, salubrinal, or phenazine (PubMed:26744324). Produced by alternative splicing and the skipping of exon 4. Produced by alternative splicing, which results in the retention of exon 4. Belongs to the AAA ATPase family. Spastin subfamily. Lacks the conserved MIT domain, which is one of the features of the spastin family.