St. Jude study shows motor protein prestin is critical for mammals' hearingSt. Jude Children's Research Hospital (ALSAC) Cell membrane protein is key in sound amplification The study was a collaboration among investigators at St. Jude, Harvard and Boys Town National Research Hospital. The mammalian inner ear contains an amplifier that increases its sensitivity to sounds. The identity of this amplifier has been elusive for half a century. Previous research, however, has suggested the amplification depends on the outer hair cells in the cochlea changing their lengths in response to voltage changes. Zuo and his colleagues now prove prestin is the molecular motor that enables these cells to change length. The study showed mice without the gene that expresses prestin experienced a 40-60 decibel loss of cochlear sensitivity. "This level of hearing, which is several hundred times less sensitive than in mice with prestin, is precisely what you'd expect with no amplifier," Zuo said. Furthermore, by studying mice with two, one and zero copies of the gene expressing prestin, Zuo and his colleagues have shown there is a surprisingly simple correlation between outer hair cell motility and amplification. The mice with only one copy of the prestin gene show precisely half of the prestin, outer hair cell motility and ability to amplify and hear sounds. "This is the strongest evidence that prestin-mediated motility is the source of amplification and that no other mechanisms exist," Zuo said. "Nature works in simple and beautiful ways." According to Zuo, prestin is not important simply for our general understanding of hearing. Mutations in the prestin gene also likely cause human deafness.
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