( rs to dominate the amplification proces...)St. Jude study solves mystery of mammalian ears

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.