ATP-dependent microtubule severing protein. Severs microtubules along their length and depolymerizes their ends, primarily the minus-end, suppressing microtubule growth from and attachment to centrosomes. Microtubule severing may promote rapid reorganization of cellular microtubule arrays and the release of microtubules from the centrosome following nucleation. Microtubule release from the mitotic spindle poles may allow depolymerization of the microtubule end proximal to the spindle pole, leading to poleward microtubule flux and poleward motion of chromosome (By similarity). Interacts with AKAP8 (via C-terminus). Localizes to centrosomes throughout mitosis and to the spindle midzone during telophase. Widely expressed. Expression begins in the embryo at 8.5 dpc. Oocyst, optic cup and pelvic anlage show strongest expression. At 10.5 dpc, expression concentrated in epithelial cells of the dorso-lateral, posterior and anterior otocyst wall. Expression in the eye is found fairly evenly throughout the retinal neural epithelium, with some enrichment in the inner retina where cells begin their differentiation to form retinal ganglion cells. Some expression is seen in the lens pit and in the cell layer that will become the pigment epithelium. At 11.5 dpc, when the superior semicircular canal has begun to form from the posterior otocyst, much of the expression is concentrated there, although there is also expression in the part of the otocyst that will form the lateral or horizontal canal. Strong expression was also seen in the acoustic ganglia and cochlea. In the eye the expression pattern is similar to that found in 10.5 dpc except that expression is concentrated in the retinal ganglion layer. As the lens vesicle forms and matures at 13 dpc, expression is also seen in the anterior wall of the lens, but persists throughout the neural retina, especially in the peripheral retina where cells are still differentiating. Defects in Fign are characterized by a side-to-side head-shaking and circling behavior, due to reduced or absent semicircular canals. Diseased mice also have small eyes, associated with cell-cycle delay and insufficient growth of the retinal neural epithelium, and lower penetrance skeletal abnormalities, including pelvic girdle dysgenesis, skull bone fusions and polydactyly. FIGN and AKAP8 double mutant mice die soon after birth due to cleft palate. Belongs to the AAA ATPase family.