This report deals with the as yet undetermined issue of whether cell-surface associated microtubules in certain cochlear epithelial cells are centrosomally nucleated and subsequently migrate to microtubulecapturing sites located at the surface regions in question. Alternatively, the cells may possess additional nucleating sites which are noncentrosomal and surface-associated. These alternative possibilities have been investigated for highly polarised epithelial cells called supporting cells in the mouse and guinea pig organ of Corti using antibodies to pericentrin and γ-tubulin. There is substantial evidence that both proteins are essential components of microtubule-nucleating sites in cells generally. Each mature supporting cell possesses a large microtubule array that is remotely located with respect to its centrosome (more than 10 µm away). The antibodies bind to a cell's centrosome. No binding has been detected at 2 other microtubule-organising centres that are associated with the ends of the centrosomally-remote microtubule array while it is being constructed. Such arrays include thousands of microtubules in some of the cell types that have been examined. If all a cell's microtubules are nucleated by its centrosome then the findings reported above imply that microtubules escape from the centrosomal nucleating site and migrate to a new location. Furthermore, capture of the plus and minus ends of the errant microtubules is taking place because both ends of a centrosomally-remote microtubule array are attached to sites that are precisely positioned at certain cell surface locations. Minus ends are locating targets with an exactitude comparable to that which has been demonstrated for plus ends in certain cell types. These cells apparently operate a single control centre strategy for microtubule nucleation that is complemented by precise positioning of plus and minus endcapturing sites at the cell surface.
Mature inner pillar cells in the mammalian organ of Corti are curved through about 60 degrees, where they arch over adjacent epithelial cells and the apex of an intercellular space called the tunnel of Corti. This report deals with changes in microtubule organization that are associated with cell bending and tunnel formation during morphogenesis of the mouse organ of Corti. A large bundle of up to 3,000 microtubules assembles in each inner pillar cell. Microtubule rearrangement occurs about 5 days after bundle assembly begins. The lumen of each initially straight hollow tube-shaped microtubule bundle is occluded as the bundle becomes more compact and elliptical in cross section. This event anticipates the once-only bending which subsequently occurs between particular levels (about 9-19 microns) below the top of a bundle as it curves into its final shape about 2 days later. Microtubule rearrangement presumably facilitates bending which is effected in the plane of least mechanical resistance parallel to the short axis of a bundle's elliptical cross-sectional profile. Precocious bending of bundles has been induced about 1.5 days in advance of the natural event. Abnormal positioning of these prematurely curved bundles indicates that bending is effected by a contractile mechanism located within bundles rather than being a response to externally applied forces. The potential importance of such microtubule-associated contractions for active modulation of the vibratory response in the cochlea during hearing is considered.
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