PROLONGED PHOTORESPONSES IN TRANSGENIC MOUSE RODS LACKING ARRESTIN

Arrestins are soluble cytoplasmic proteins that bind to G-protein-coup led receptors, thus switching off activation of the G protein and term inating the signalling pathway that triggers the cellular response(1,2 ). Although visual arrestin has been shown to quench the catalytic act ivity of photoexcited, phosphorylated rhodopsin in a reconstituted sys tem(3), its role in the intact rod cell remains unclear because phosph orylation alone reduces the catalytic activity of rhodopsin(4-6). Here we have recorded photocurrents of rods from transgenic mice in which one or both copies of the arrestin gene were disrupted, Photoresponses were unaffected when arrestin expression was halved, indicating that arrestin binding is not rate limiting for recovery of the rod photores ponse, as it is in Drosophila(7,8). With arrestin absent, the flash re sponse displayed a rapid partial recovery followed by a prolonged fina l phase, This behaviour indicates that an arrestin-independent mechani sm initiates the quench of rhodopsin's catalytic activity and that arr estin completes the quench, The intensity dependence of the photorespo nse in rods lacking arrestin further suggests that, although arrestin is required for normal signal termination, it does not participate dir ectly in light adaptation.