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J Biol Chem. 2015 Apr 3;290(14):9239-50. doi: 10.1074/jbc.M115.639591. Epub 2015 Feb 11.

Regulation of mammalian cone phototransduction by recoverin and rhodopsin kinase.

Author information

1
From the Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63110.
2
the Zilkha Neurogenetic Institute, Department of Cell and Neurobiology & Department of Ophthalmology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, and.
3
the Schepens Eye Research Institute and Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts 02114.
4
From the Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63110, kefalov@vision.wustl.edu.

Abstract

Cone photoreceptors function under daylight conditions and are essential for color perception and vision with high temporal and spatial resolution. A remarkable feature of cones is that, unlike rods, they remain responsive in bright light. In rods, light triggers a decline in intracellular calcium, which exerts a well studied negative feedback on phototransduction that includes calcium-dependent inhibition of rhodopsin kinase (GRK1) by recoverin. Rods and cones share the same isoforms of recoverin and GRK1, and photoactivation also triggers a calcium decline in cones. However, the molecular mechanisms by which calcium exerts negative feedback on cone phototransduction through recoverin and GRK1 are not well understood. Here, we examined this question using mice expressing various levels of GRK1 or lacking recoverin. We show that although GRK1 is required for the timely inactivation of mouse cone photoresponse, gradually increasing its expression progressively delays the cone response recovery. This surprising result is in contrast with the known effect of increasing GRK1 expression in rods. Notably, the kinetics of cone responses converge and become independent of GRK1 levels for flashes activating more than ∼1% of cone pigment. Thus, mouse cone response recovery in bright light is independent of pigment phosphorylation and likely reflects the spontaneous decay of photoactivated visual pigment. We also find that recoverin potentiates the sensitivity of cones in dim light conditions but does not contribute to their capacity to function in bright light.

KEYWORDS:

Animal Model; Calcium-binding Protein; Cone Photoreceptors; G Protein-coupled Receptor (GPCR); Light Adaptation; Photoreceptor; Phototransduction; Recoverin; Rhodopsin Kinase

PMID:
25673692
PMCID:
PMC4423708
DOI:
10.1074/jbc.M115.639591
[Indexed for MEDLINE]
Free PMC Article

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