While both mammals and non-mammals have cilia on their outer hair cells, only mammalian outer hair cells have prestin, which drives this cellular contraction, or somatic motility. The contraction pulls the tufts of cilia downward, which maximizes the force of their vibration. In mammals, both the cilia and the cell itself vibrate. Thus far the question has been whether the cilia are the main engine of sound amplification in both mammals and non-mammals.
One group of scientists believes that somatic motility in mammalian outer hair cells is simply a way to change the height of the cilia in the fluid to maximize the force with which the cilia oscillate. That, in turn, would amplify the sound. An opposing group of scientists maintains that although the vibration of the outer hair cell body itself—somatic motility—does maximize the vibration of the cilia, the cell body works independently of its cilia. That is, vibration of the mammalian cell dominates the work of amplifying sound in mammals.
“If somatic motility is the dominant force for amplifying sound in mammals, this would mean that prestin is the reason mammals amplify sound so efficiently,” Zuo said.
In the current study, Zuo and his team conducted a complex series of studies that showed in mammals that the role of somatic mobility driven by prestin is not simply to modify the response of the outer hair cells’ cilia to incoming sound waves in the cochlea fluid. Instead, somatic motility itself appears to dominate the amplification process in the mammalian cochlea, while the cilia dominate amplification in non-mammals.
Zuo’s team took advantage of a previously discovered mutated form of prestin that does not make the outer hair cells contract in response to incoming sound waves as normal prestin does. Instead, the mutated form of prestin makes the cell extend itself when it vibrates.
The St. Jude researchers reasoned that if altering the position of the cilia in the fluid changes the ability of the cilia to amplify sound, then hearing should be affected when the mutant prestin made the cell extend itself. Therefore, the team developed a line of genetically modified mice that carried only mutant prestin in their outer hair cells. The researchers then tested the animals’ responses to sound.
Results of the studies showed no alteration in hearing, which suggested that it did not matter whether the outer hair cells contracted or extended itself, that is, raised or lowered the cilia. There was no effect on amplification. The researchers concluded that somatic motility was not simply a way to make cilia do their job better; rather, there is no connection between the hair cell contractions and how the cilia do their job. Instead, somatic motility, generated by prestin, is the key to the superior hearing of mammals.
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Other authors of this study include Jiangang Gao, Xudong Wu and Manish Patel (St. Jude); Xiang Wang, Shuping Jia and David He (Creighton University, Omaha, Neb.); Sal Aguinaga, Kristin Huynh, Keiji Matsuda, Jing Zheng, MaryAnn Cheatham and Peter Dallos (Northwestern University, Evanston, Ill.).
This work was supported in part by ALSAC, The Hugh Knowles Center and the National Institutes of Health.
St. Jude Children's Research Hospital
St. Jude Children's Research Hospital is internationally recognized for its pioneering work in finding cures and saving children with cancer and other catastrophic diseases. Founded by late entertainer Danny Thomas and based in Memphis, Tenn., St. Jude freely shares its discoveries with scientific and medical communities around the world. No family ever pays for treatments not covered by insurance, and families without insurance are never asked to pay. St. Jude is financially supported by ALSAC, its fundraising organization. For more information, please visit www.stjude.org. |
