"It might be possible one day to screen a person for susceptibility to hearing loss by measuring the level of Ink4d they have," Segil said. "We could use that information to warn people they are at increased risk for hearing loss due to trauma."

The requirement that these cells must remain "quiet" (not divide) may mean that gene therapy aimed at replacing lost sensory hair cells through cell division to restore hearing might only stimulate these cells to try undergo apoptosis and die, thus worsening the condition, according to Martine Roussel, Ph.D., a co-author of the paper reporting these results and a member of the St. Jude Department of Genetics and Tumor Cell Biology, and a professor in the Department of Molecular Sciences at the University of Tennessee (Memphis).

Sensory hair cells respond to sound waves by setting off electric impulses in nerves that help generate the sense of hearing. Rows of these cells form during development of the embryo and, together with other cells called supporting cells, make up the organ of Corti in the inner ear, according to Roussel. These cells normally do not multiply after they are formed in the embryo; therefore, they can't multiply to replace lost or damaged sensory hair cells later in life. However, in the absence of Ink4d, they may attempt to divide.

"In fact, in the mice that lacked Ink4d, hair cells sometimes tried to divide," Roussel said. "This led to apoptosis and hearing loss in these mice."

The dominant role of Ink4d in sensory hair cells is unique. In other parts of the brain, nerve cell division is controlled in part by either Ink4d or by another gene, Kip1. In these cells, the loss of either gene does not completely take the brakes off of cell division. However, the researchers fo
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Contact: Bonnie Cameron
bonnie.cameron@stjude.org
901-495-4815
St. Jude Children's Research Hospital
1-May-2003