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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-176

Rinner, O; Makhankov, Y V; Biehlmaier, O; Neuhauss, S C F (2005). Knockdown of cone-specific kinase GRK7 in larval zebrafish leads to impaired cone response recovery and delayed dark adaptation. Neuron, 47(2):231-242.

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Abstract

Phosphorylation of rhodopsin by rhodopsin kinase GRK1 is an important desensitization mechanism in scotopic vision. For cone vision GRK1 is not essential. However, cone opsin is phosphorylated following light stimulation. In cone-dominant animals as well as in humans, but not in rodents, GRK7, a cone-specific homolog of GRK1, has been identified in cone outer segments. To investigate the function of GRK7 in vivo, we cloned two orthologs of grk7 in zebrafish and knocked down gene expression of grk7a in zebrafish larvae by morpholino antisense nucleotides. Photoresponse recovery in Grk7a-deficient larvae was delayed in electroretinographic measurements, and temporal contrast sensitivity was reduced, particularly under bright-light conditions. These results show that function of a cone-specific kinase is essential for cone vision in the zebrafish retina and argue that pigment bleaching and spontaneous decay alone are not sufficient for light adaptation and rapid cone response inactivation.

Item Type:Journal Article, refereed, original work
Communities & Collections:07 Faculty of Science > Institute of Molecular Life Sciences
DDC:570 Life sciences; biology
Language:English
Date:21 July 2005
Deposited On:11 Feb 2008 13:13
Last Modified:28 Nov 2013 01:09
Publisher:Elsevier
ISSN:0896-6273
Publisher DOI:10.1016/j.neuron.2005.06.010
PubMed ID:16039565
Citations:Web of Science®. Times Cited: 30
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