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dc.contributor.authorHu, Wen
dc.contributor.authorWan, Didi
dc.contributor.authorYu, Xiaoming
dc.contributor.authorCao, Jinguo
dc.contributor.authorGuo, Peiyi
dc.contributor.authorLi, Hong-Sheng
dc.contributor.authorHan, Junhai
dc.date2022-08-11T08:09:29.000
dc.date.accessioned2022-08-23T16:32:22Z
dc.date.available2022-08-23T16:32:22Z
dc.date.issued2012-04-20
dc.date.submitted2013-01-23
dc.identifier.citationJ Biol Chem. 2012 Apr 20;287(17):13911-8. doi: 10.1074/jbc.M112.339895. <a href="http://dx.doi.org/10.1074/jbc.M112.339895">Link to article on publisher's site</a>
dc.identifier.issn0021-9258 (Linking)
dc.identifier.doi10.1074/jbc.M112.339895
dc.identifier.pmid22389492
dc.identifier.urihttp://hdl.handle.net/20.500.14038/37872
dc.description<p>Co-author Peiyi Guo is a doctoral student in the Neuroscience Program in the Graduate School of Biomedical Sciences (GSBS) at UMass Medical School.</p>
dc.description.abstractAppropriate termination of the phototransduction cascade is critical for photoreceptors to achieve high temporal resolution and to prevent excessive Ca(2+)-induced cell toxicity. Using a genetic screen to identify defective photoresponse mutants in Drosophila, we isolated and identified a novel Galpha(q) mutant allele, which has defects in both activation and deactivation. We revealed that G(q) modulates the termination of the light response and that metarhodopsin/G(q) interaction affects subsequent arrestin-rhodopsin (Arr2-Rh1) binding, which mediates the deactivation of metarhodopsin. We further showed that the Galpha(q) mutant undergoes light-dependent retinal degeneration, which is due to the slow accumulation of stable Arr2-Rh1 complexes. Our study revealed the roles of G(q) in mediating photoresponse termination and in preventing retinal degeneration. This pathway may represent a general rapid feedback regulation of G protein-coupled receptor signaling.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=22389492&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1074/jbc.M112.339895
dc.subjectAlleles
dc.subjectAnimals
dc.subjectAnimals, Genetically Modified
dc.subjectArrestins
dc.subjectDrosophila Proteins
dc.subjectDrosophila melanogaster
dc.subjectElectrophysiology
dc.subjectGTP-Binding Protein alpha Subunits, Gq-G11
dc.subjectLight
dc.subjectLight Signal Transduction
dc.subjectModels, Genetic
dc.subjectMutation
dc.subjectPhotoreceptor Cells, Invertebrate
dc.subjectReceptors, G-Protein-Coupled
dc.subjectRetinal Degeneration
dc.subjectRhodopsin
dc.subjectBiochemistry, Biophysics, and Structural Biology
dc.subjectNeuroscience and Neurobiology
dc.titleProtein Gq modulates termination of phototransduction and prevents retinal degeneration
dc.typeJournal Article
dc.source.journaltitleThe Journal of biological chemistry
dc.source.volume287
dc.source.issue17
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/neurobiology_pp/142
dc.identifier.contextkey3608536
html.description.abstract<p>Appropriate termination of the phototransduction cascade is critical for photoreceptors to achieve high temporal resolution and to prevent excessive Ca(2+)-induced cell toxicity. Using a genetic screen to identify defective photoresponse mutants in Drosophila, we isolated and identified a novel Galpha(q) mutant allele, which has defects in both activation and deactivation. We revealed that G(q) modulates the termination of the light response and that metarhodopsin/G(q) interaction affects subsequent arrestin-rhodopsin (Arr2-Rh1) binding, which mediates the deactivation of metarhodopsin. We further showed that the Galpha(q) mutant undergoes light-dependent retinal degeneration, which is due to the slow accumulation of stable Arr2-Rh1 complexes. Our study revealed the roles of G(q) in mediating photoresponse termination and in preventing retinal degeneration. This pathway may represent a general rapid feedback regulation of G protein-coupled receptor signaling.</p>
dc.identifier.submissionpathneurobiology_pp/142
dc.contributor.departmentGraduate School of Biomedical Sciences, Neuroscience Program
dc.contributor.departmentLi Lab
dc.contributor.departmentNeurobiology
dc.source.pages13911-8
dc.contributor.studentPeiyi Guo
dc.description.thesisprogramNeuroscience


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