The electromotility of cochlear outer hair cells (OHCs) is a required process for normal hearing, and involves a membrane-based mechanism in which the transmembrane protein, prestin, plays a central role. We have investigated the contribution of prestin to the mechanics and electromechanics of the cell membrane using membrane tethers formed from human embryonic kidney cells. Our results suggest that prestin appears to change membrane tension and amplify electrically-evoked force generation, while a single point mutation of alanine to tryptophan in prestin reduces electrically-evoked force generation without affecting the membrane tension. We propose that prestin and membrane work in synergy to produce the electrical and mechanical changes that are required during OHC electromotility.