Researchers Discover Mechanism Underlying Stereocilia Self-Renewal
April 19, 2004
Size is important. This is according to NIDCD scientists* investigating the internal mechanisms that underlie the hearing process and how the structures responsible for hearing rebuild themselves. This study is published in the March 15, 2004 issue of The Journal of Cell Biology.
Hearing happens at the level of the hair cells of the ear--the basic sensory elements of hearing--where sound energy is transformed into electrical energy by tiny hairlike projections jutting from the top of cells in bundles called stereocilia. The cells are called "hair cells" because of their appearance and these structures can only be seen with powerful microscopes. Stereocilia are arranged in varying lengths, similar to a stack of soda straws graded in height forming a staircase-like bundle, to accommodate the different energies found in different frequencies of sound waves. When stimulated, the stereocilia bundle moves and the individual hair cells splay apart, which creates an electrical signal that travels to the brain by way of the auditory nerve, allowing hearing to take place. The bending action can cause damage to the stereocilia, but a delicate mechanism of turnover replaces the components of stereocilia in an orderly manner to minimize injury.
Researchers have looked at various factors that control and regulate the rate of repair or turnover that takes place in stereocilia. In this study, they found that the turnover rate is determined by size--longer stereocilia are replaced at a faster rate than shorter ones. The stereocilia, which are largely made up of the building block protein, actin, rebuilds itself continuously, maintaining the overall structure. The scientists theorize that this activity may help maintain function over the course of a lifetime.
How this turnover mechanism is regulated remains unknown, but the researchers noted that the levels and activity of another protein, myosin, are correlated with stereocilia length in genetically-altered mice. Mutations in the gene for myosin are known to prevent stereocilia elongation. The investigators say they will continue to look for other proteins in order to identify key players in the self-renewal mechanism and interactions between them. They believe that understanding how malfunctions occur in the ability of the hair cell bundle to make fine changes in their lengths may account for subtle changes in hearing. Moreover, long-term applications of this research may prove important in the development of treatments for temporary and permanent hearing loss due to stereocilia injury.
*Section on Structural Cell Biology, National Institute on Deafness and Other Communication Disorders, National Institutes of Health
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