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Publication : Control of rhodopsin's active lifetime by arrestin-1 expression in mammalian rods.

First Author  Gross OP Year  2010
Journal  J Neurosci Volume  30
Issue  9 Pages  3450-7
PubMed ID  20203204 Mgi Jnum  J:159020
Mgi Id  MGI:4441079 Doi  10.1523/JNEUROSCI.5391-09.2010
Citation  Gross OP, et al. (2010) Control of rhodopsin's active lifetime by arrestin-1 expression in mammalian rods. J Neurosci 30(9):3450-7
abstractText  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 twofold 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 approximately 40 ms in wild-type mouse rods, much faster than previous estimates.
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