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Knockdown of Cone-Specific Kinase GRK7 in Larval Zebrafish Leads to Impaired Cone Response Recovery and Delayed Dark Adaptation
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 con...
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Published in: | Neuron (Cambridge, Mass.) Mass.), 2005-07, Vol.47 (2), p.231-242 |
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description | 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. |
doi_str_mv | 10.1016/j.neuron.2005.06.010 |
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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.</description><identifier>ISSN: 0896-6273</identifier><identifier>EISSN: 1097-4199</identifier><identifier>DOI: 10.1016/j.neuron.2005.06.010</identifier><identifier>PMID: 16039565</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Animals, Genetically Modified ; Arrestin - metabolism ; Blotting, Western ; Cloning ; Cloning, Molecular - methods ; Contrast Sensitivity - genetics ; Contrast Sensitivity - physiology ; Danio rerio ; Dark Adaptation - genetics ; Electroretinography - methods ; Endocrine system ; Evoked Potentials - genetics ; Evoked Potentials - radiation effects ; Eye - metabolism ; Eye - pathology ; Freshwater ; G-Protein-Coupled Receptor Kinases ; Gene Expression Regulation, Developmental ; Genomes ; Immunohistochemistry - methods ; In Situ Hybridization - methods ; Kinases ; Larva - genetics ; Larva - physiology ; Light ; Phosphorylation ; Photic Stimulation - methods ; Photoreceptors ; Pineal Gland - embryology ; Pineal Gland - metabolism ; Protein-Serine-Threonine Kinases - deficiency ; Protein-Serine-Threonine Kinases - physiology ; Psychophysics ; Retina ; Retinal Cone Photoreceptor Cells - embryology ; Retinal Cone Photoreceptor Cells - metabolism ; Retinal Cone Photoreceptor Cells - physiology ; Rhodopsin - metabolism ; Time Factors ; Zebrafish ; Zebrafish - genetics ; Zebrafish - physiology ; Zebrafish Proteins</subject><ispartof>Neuron (Cambridge, Mass.), 2005-07, Vol.47 (2), p.231-242</ispartof><rights>2005 Elsevier Inc.</rights><rights>Copyright Elsevier Limited Jul 21, 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c531t-1ce8911fbdc5fd6c8fd5405886b1acc910defa21eeed0a69ff0d868292cb565a3</citedby><cites>FETCH-LOGICAL-c531t-1ce8911fbdc5fd6c8fd5405886b1acc910defa21eeed0a69ff0d868292cb565a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16039565$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rinner, Oliver</creatorcontrib><creatorcontrib>Makhankov, Yuri V.</creatorcontrib><creatorcontrib>Biehlmaier, Oliver</creatorcontrib><creatorcontrib>Neuhauss, Stephan C.F.</creatorcontrib><title>Knockdown of Cone-Specific Kinase GRK7 in Larval Zebrafish Leads to Impaired Cone Response Recovery and Delayed Dark Adaptation</title><title>Neuron (Cambridge, Mass.)</title><addtitle>Neuron</addtitle><description>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. 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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.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16039565</pmid><doi>10.1016/j.neuron.2005.06.010</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Animals, Genetically Modified Arrestin - metabolism Blotting, Western Cloning Cloning, Molecular - methods Contrast Sensitivity - genetics Contrast Sensitivity - physiology Danio rerio Dark Adaptation - genetics Electroretinography - methods Endocrine system Evoked Potentials - genetics Evoked Potentials - radiation effects Eye - metabolism Eye - pathology Freshwater G-Protein-Coupled Receptor Kinases Gene Expression Regulation, Developmental Genomes Immunohistochemistry - methods In Situ Hybridization - methods Kinases Larva - genetics Larva - physiology Light Phosphorylation Photic Stimulation - methods Photoreceptors Pineal Gland - embryology Pineal Gland - metabolism Protein-Serine-Threonine Kinases - deficiency Protein-Serine-Threonine Kinases - physiology Psychophysics Retina Retinal Cone Photoreceptor Cells - embryology Retinal Cone Photoreceptor Cells - metabolism Retinal Cone Photoreceptor Cells - physiology Rhodopsin - metabolism Time Factors Zebrafish Zebrafish - genetics Zebrafish - physiology Zebrafish Proteins |
title | Knockdown of Cone-Specific Kinase GRK7 in Larval Zebrafish Leads to Impaired Cone Response Recovery and Delayed Dark Adaptation |
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