Control of rhodopsin's active lifetime by arrestin-1 expression in mammalian rods.
Control of rhodopsin's active lifetime by arrestin-1 expression in mammalian rods.
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DOI：
10.1523/jneurosci.5391-09.2010
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发表时间：
2010-03-03
期刊：
影响因子：
--
通讯作者：
Burns ME
中科院分区：
文献类型：
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作者：
Gross OP;Burns ME
在杆状光感受器中，光激活的g蛋白偶联受体视紫红质（R*）的失活由磷酸化启动，并通过随后的视觉抑制蛋白（Arr1）结合完成。由于R*寿命比下游G蛋白和效应分子的寿命短得多，这些个体相互作用的体内动力学已被证明难以精确确定。在这里，我们使用具有加速下游失活动力学的转基因小鼠系来揭示Arr1结合对视紫红质失活的总体时间过程的贡献。光响应显示，在表达正常Arr1量的一半的杆中，R*的寿命显着增加，这与在大范围闪光强度下Arr1结合速率降低两倍的方式一致。与已建立的光受体生物化学相一致的光反应失活的基本模型表明，在野生型小鼠棒中，R*磷酸化和Arr1结合发生的时间常数为~ 40 ms，比以前的估计要快得多。
In rod photoreceptors, deactivation of the light-activated G-protein-coupled receptor rhodopsin (R*) is initiated by phosphorylation and completed through subsequent binding of visual arrestin (Arr1). The in vivo kinetics of these individual interactions have proven difficult to determine with precision since R* lifetime is much shorter than the lifetimes of downstream G protein and effector molecules. Here, we have used a transgenic mouse line with accelerated downstream deactivation kinetics to reveal the contribution of Arr1 binding to the overall time course of rhodopsin deactivation. Photoresponses revealed that the lifetime of R* is significantly increased in rods that express half of the normal amount of Arr1, in a manner consistent with a two-fold decrease in the rate of Arr1 binding across a wide range of flash strengths. A basic model of photoresponse deactivation consistent with established photoreceptor biochemistry shows that R* phosphorylation and Arr1 binding occur with a time constant of ∼40 ms in wild-type mouse rods, much faster than previous estimates.