Prestin’s fast motor kinetics is essential for mammalian cochlear amplification

Author:

Takahashi Satoe1ORCID,Zhou Yingjie2,Kojima Takashi1,Cheatham Mary Ann23ORCID,Homma Kazuaki13ORCID

Affiliation:

1. Department of Otolaryngology–Head and Neck Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611

2. Department of Communication Sciences and Disorders, Northwestern University, Evanston, IL 60208

3. The Hugh Knowles Center for Clinical and Basic Science in Hearing and Its Disorders, Northwestern University, Evanston, IL 60208

Abstract

Prestin (SLC26A5)-mediated voltage-driven elongations and contractions of sensory outer hair cells within the organ of Corti are essential for mammalian cochlear amplification. However, whether this electromotile activity directly contributes on a cycle-by-cycle basis is currently controversial. By restoring motor kinetics in a mouse model expressing a slowed prestin missense variant, this study provides experimental evidence acknowledging the importance of fast motor action to mammalian cochlear amplification. Our results also demonstrate that the point mutation in prestin disrupting anion transport in other proteins of the SLC26 family does not alter cochlear function, suggesting that the potential weak anion transport of prestin is not essential in the mammalian cochlea.

Funder

HHS | NIH | National Institute on Deafness and Other Communication Disorders

Publisher

Proceedings of the National Academy of Sciences

Subject

Multidisciplinary

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