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

Owen P. Gross, Marie E Burns

Research output: Contribution to journalArticle

53 Scopus citations

Abstract

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 ismuchshorter 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 ∼40 ms in wild-type mouse rods, much faster than previous estimates.

Original languageEnglish (US)
Pages (from-to)3450-3457
Number of pages8
JournalJournal of Neuroscience
Volume30
Issue number9
DOIs
StatePublished - Mar 3 2010

ASJC Scopus subject areas

  • Neuroscience(all)

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