Injury-Induced Remodeling of Junctional Actin Bands in the Vestibular Maculae of Mice and Chicks: Implications for Sensory Regeneration

The vestibular organs of birds are capable of regenerating sensory hair cells after ototoxic injury, but the regenerative ability of the mammalian vestibular organs is much more limited. The factors that inhibit regeneration in the mammalian inner ear are not known, but it has been proposed that the structure of filamentous actin cables at cell-cell junctions within the sensory epithelium may be an important regulatory influence. Junctional actin cables in the chick utricle are relatively thin, while those in mouse utricle are much thicker. These differences result in differing mechanical properties of the avian vs. mammalian inner ear, which may affect the potential for regenerative proliferation. The present study characterized injury-evoked changes in junctional actin cables in the utricles of mice and chicks. We found that the thickness of junctional cables in the chick utricle was not affected by ototoxic injury, but that injury to the mouse utricle led to the formation of many new junctional actin bands whose thickness was comparable to those in the chick utricle. Thicker actin bands persisted after injury, but were not necessarily associated with cellular junctions. In addition, the relative extent of supporting cell expansion in the injured chick utricle was larger than that in the mouse utricle, which may affect activation of Hippo/YAP signaling in both species. Together, these data point to important differences in actin cable plasticity in the avian vs. mammalian utricle that may partially account for their differing regenerative abilities.