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
Top
|
 |
|
