| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||




* Applied Physics Graduate Program,
Department of Bioengineering, Rice University, Houston, Texas;
Bobby R. Alford Department of Otolaryngology Head and Neck Surgery,
Huffington Center on Aging, Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas; and ¶ Department of Bioengineering, University of California, Riverside, California
Correspondence: Address reprint requests and inquiries to Bahman Anvari, Tel.: 951-827-5726; E-mail: anvari{at}engr.ucr.edu.
The voltage-dependent movement, or electromotility, of cochlear outer hair cells contributes to cochlear amplification in mammalian hearing. Outer hair-cell electromotility involves a membrane-based motor in which the membrane protein prestin plays a central role. We have investigated the contribution of prestin to the mechanics and electromechanical force (EMF) generation of the membrane using membrane tethers formed from human embryonic kidney (HEK) cells. Several measures of membrane tether mechanics are greater in tethers pulled from HEK cells transfected with prestin when compared to control untransfected HEK cells. A single point mutation of alanine to tryptophan (A100W) in prestin eliminates prestin-associated charge movement and diminishes EMF but does not alter passive membrane mechanics. These results suggest that prestin-associated charge transfer is necessary for maximal EMF generation by the membrane.
This article has been cited by other articles:
![]() |
M. Drexl, M. M. Mellado Lagarde, J. Zuo, A. N. Lukashkin, and I. J. Russell The Role of Prestin in the Generation of Electrically Evoked Otoacoustic Emissions in Mice J Neurophysiol, April 1, 2008; 99(4): 1607 - 1615. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |