Mouse cones require an arrestin for normal inactivation of phototransduction

被引：118

作者：

Nikonov, Sergei S. ^{[1
]}

Brown, Bruce M. ^{[2
,3
]}

Davis, Jason A. ^{[1
]}

Zuniga, Freddi I. ^{[2
,3
]}

Bragin, Alvina ^{[1
]}

Pugh, Edward N., Jr. ^{[1
]}

Craft, Cheryl M. ^{[2
,3
,4
]}

机构：

[1] Univ Penn, Dept Ophthalmol, Sch Med, FM Kirby Ctr Mol Ophthalmol, Philadelphia, PA 19104 USA

[2] Doheny Eye Inst, Mary D Allen Lab Vis Res, Los Angeles, CA 90033 USA

[3] Univ So Calif, Dept Ophthalmol, Los Angeles, CA 90033 USA

[4] Univ So Calif, Dept Cell & Neurobiol, Keck Sch Med, Los Angeles, CA 90033 USA

来源：

NEURON | 2008年 / 59卷 / 03期

关键词：

D O I：

10.1016/j.neuron.2008.06.011

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Arrestins are proteins that arrest the activity of G protein-coupled receptors (GPCRs). While it is well established that normal inactivation of photoexcited rhodopsin, the GPCR of rod phototransduction, requires arrestin (Arr1), it has been controversial whether the same requirement holds for cone opsin inactivation. Mouse cone photoreceptors express two distinct visual arrestins: Arr1 and Arr4. By means of recordings from cones of mice with one or both arrestins knocked out, this investigation establishes that a visual arrestin is required for normal cone inactivation. Arrestin-independent inactivation is 70-fold more rapid in cones than in rods, however. Dual arrestin expression in cones could be a holdover from ancient genome duplication events that led to multiple isoforms of arrestin, allowing evolutionary specialization of one form while the other maintains the basic function.

引用

页码：462 / 474

页数：13

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