0000000000624433

AUTHOR

W. Clay Smith

showing 3 related works from this author

Photoreceptor vitality in organotypic cultures of mature vertebrate retinas validated by light-dependent molecular movements

2006

AbstractVertebrate photoreceptor cells are polarized neurons highly specialized for light absorption and visual signal transduction. Photoreceptor cells consist of the light sensitive outer segment and the biosynthetic active inner segment linked by a slender connecting cilium. The function of mature photoreceptor cells is strictly dependent on this compartmentalization which is maintained in the specialized retinal environment. To keep this fragile morphologic and functional composition for further cell biological studies and treatments we established organotypic retina cultures of mature mice and Xenopus laevis. The organotypic retina cultures of both model organisms are created as co-cul…

Photoreceptorsgenetic structuresMouseXenopusCellved/biology.organism_classification_rank.speciesXenopusGene deliverySignal transductionRetinaMicechemistry.chemical_compoundOrgan Culture TechniquesOrganotypic retina cultureIn Situ Nick-End LabelingmedicineAnimalsPhotoreceptor CellsTransducinModel organismVision OcularRetinaArrestinbiologyved/biologyRetinalbiology.organism_classificationLight-dependent movementsSensory Systemseye diseasesCell biologyMice Inbred C57BLProtein TransportOphthalmologymedicine.anatomical_structureMicroscopy FluorescencechemistryCell cultureVertebratesTransducinsense organsPhotic StimulationVision Research
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AAV-Mediated Clarin-1 Expression in the Mouse Retina: Implications for USH3A Gene Therapy

2015

Usher syndrome type III (USH3A) is an autosomal recessive disorder caused by mutations in clarin-1 (CLRN1) gene, leading to progressive retinal degeneration and sensorineural deafness. Efforts to develop therapies for preventing photoreceptor cell loss are hampered by the lack of a retinal phenotype in the existing USH3 mouse models and by conflicting reports regarding the endogenous retinal localization of clarin-1, a transmembrane protein of unknown function. In this study, we used an AAV-based approach to express CLRN1 in the mouse retina in order to determine the pattern of its subcellular localization in different cell types. We found that all major classes of retinal cells express AAV…

Photoreceptors0301 basic medicineRetinal degenerationSensory ReceptorsPhysiologyUsher syndromeCell Membraneslcsh:MedicineSocial SciencesNervous SystemPhotoreceptor cellMicechemistry.chemical_compound0302 clinical medicineAnimal CellsMedicine and Health SciencesPsychologylcsh:ScienceNeuronsRegulation of gene expressionGeneticsMultidisciplinaryRetinal DegenerationAnimal ModelsDependovirusCell biologyElectrophysiologymedicine.anatomical_structureSensory PerceptionCellular TypesAnatomyCellular Structures and OrganellesUsher SyndromesResearch ArticleSignal TransductionCell typeImaging TechniquesOcular AnatomyNeurophysiologyOuter plexiform layerMouse ModelsBiologyResearch and Analysis MethodsRetina03 medical and health sciencesModel OrganismsOcular SystemFluorescence ImagingmedicineAnimalsHumansRetinalcsh:RMembrane ProteinsBiology and Life SciencesAfferent NeuronsRetinalGenetic TherapyCell Biologymedicine.diseaseDisease Models Animal030104 developmental biologyGene Expression RegulationchemistrySynapsesEyeslcsh:QHead030217 neurology & neurosurgeryNeurosciencePLOS ONE
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Light-Dependent Translocation of Arrestin in Rod Photoreceptors is Signaled through a Phospholipase C Cascade and Requires ATP

2009

Light adaptation of rod photoreceptors induces translocation of arrestin from inner segments (IS) to outer segments (OS). Our study suggests that components of the G-protein linked phosphoinositide pathway play a role in signaling the initiating events of arrestin translocation. We show that arrestin translocation can be stimulated by activators of phospholipase C (PLC) and protein kinase C (PKC) in the absence of light. Conversely, arrestin translocation to the OS is significantly slowed by inhibitors of PLC and PKC.In the second part of this study, we investigated the mechanism by which arrestin translocates in response to light. Other investigators have suggested that arrestin translocat…

Cholera ToxinLightgenetic structuresG proteinBiophysicsXenopusChromosomal translocationBiologyPhosphatidylinositolsArticleMiceXenopus laevisAdenosine TriphosphateRetinal Rod Photoreceptor CellsArrestinAnimalsEnzyme InhibitorsPotassium CyanideCells CulturedProtein Kinase CProtein kinase CArrestinPhosphoinositide PathwayPhospholipase CChemistryCell Biologybiology.organism_classificationeye diseasesCell biologyRhodopsinType C Phospholipasesbiology.proteinPhosphorylationArrestin beta 2Arrestin beta 1sense organsSignal transductionSignal TransductionBiophysical Journal
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