Slc26a5 changes conformation in response to depolarization

The membrane protein Slc26a5 (prestin) contracts in the plane of the membrane in response to depolarization of the cell caused by opening of the mechanoelectric transduction (MET) channel (inferred from rat homologs). A current model for the reaction posits that association of anions (chloride or bicarbonate) with a binding pocket midway along the permeation pathway within Slc26a5 causes a change in the area occupied by Slc26a5 in the membrane. An influx of cations through the MET channel causes dissociation of anions from Slc26a5, reversing the conformational change. The contraction-elongation cycle of OHCs, due to conformational changes of Slc26a5, provides feedback-amplification of the motions (principally the reticular lamina) of the organ of Corti. At low sound levels the amplification is about a 1000-fold, decreasing nonlinearly as sound level increases. In the absence of either OHCs (Ryan and Dallos 1975) or functional Slc26a5 (Liberman et al. 2002, Cheatham et al. 2004, Dallos et al. 2008) the amplification disappears.

细胞膜蛋白Slc26a5（又称prestin）在机械电传导（MET）通道开启导致的细胞去极化作用下，在细胞膜平面发生收缩。关于此反应的当前模型推断，阴离子（如氯离子或碳酸氢根离子）与Slc26a5渗透路径中部的结合口袋的结合，会导致Slc26a5在膜中所占面积的改变。通过MET通道的阳离子内流导致阴离子从Slc26a5解离，从而逆转构象变化。由于Slc26a5的构象变化引起的听觉细胞（OHCs）的收缩-舒张周期，为Corti器官的运动（主要是网状板）提供了反馈放大。在低声级下，放大倍数约为1000倍，随着声级的增加，非线性下降。在缺乏OHCs（Ryan和Dallos，1975年）或功能正常的Slc26a5（Liberman等，2002年，Cheatham等，2004年，Dallos等，2008年）的情况下，放大效应消失。