Baylor D A, Burns M E
Department of Neurobiology, Stanford University School of Medicine, CA 94305, USA.
Eye (Lond). 1998;12 ( Pt 3b):521-5. doi: 10.1038/eye.1998.140.
Although rhodopsin's role in activating the phototransduction cascade is well known, the processes that deactivate rhodopsin, and thus the rest of the cascade, are less well understood. At least three proteins appear to play a role: rhodopsin kinase, arrestin and recoverin. Here we review recent physiological studies of the molecular mechanisms of rhodopsin deactivation. The approach was to monitor the light responses of individual mouse rods in which rhodopsin was altered or arrestin was deleted by transgenic techniques. Removal of rhodopsin's carboxy-terminal residues which contain phosphorylation sites implicated in deactivation, prolonged the flash response 20-fold and caused it to become highly variable. In rods that did not express arrestin the flash response recovered partially, but final recovery was slowed over 100-fold. These results are consistent with the notion that phosphorylation initiates rhodopsin deactivation and that arrestin binding completes the process. The stationary night blindness of Oguchi disease, associated with null mutations in the genes for arrestin or rhodopsin kinase, presumably results from impaired rhodopsin deactivation, like that revealed by the experiments on transgenic animals.
尽管视紫红质在激活光转导级联反应中的作用已广为人知，但对视紫红质失活以及由此导致的级联反应其他部分失活的过程却了解较少。至少有三种蛋白质似乎发挥了作用：视紫红质激酶、抑制蛋白和恢复蛋白。在此，我们综述了视紫红质失活分子机制的近期生理学研究。研究方法是监测通过转基因技术改变视紫红质或缺失抑制蛋白的单个小鼠视杆细胞的光反应。去除视紫红质含有与失活相关的磷酸化位点的羧基末端残基，使闪光反应延长了20倍，并使其变得高度可变。在不表达抑制蛋白的视杆细胞中，闪光反应部分恢复，但最终恢复速度减慢了100多倍。这些结果与以下观点一致，即磷酸化引发视紫红质失活，而抑制蛋白结合完成这一过程。与抑制蛋白或视紫红质激酶基因的无效突变相关的小口病静止性夜盲症，可能是由于视紫红质失活受损所致，就像转基因动物实验所揭示的那样。
