ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Modulation of mouse rod response decay by rhodopsin kinase and recoverin.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 57 citations in OpenAlex.
- The effects of bicarbonate on the aberrant photon response in murine rod photoreceptors.Biophysical journal · 2026Article
- Advantages of human opsins in optogenetic visual restoration.Frontiers in neuroscience · 2025Review
- Analysis of dim-light responses in rod and cone photoreceptors with altered calcium kinetics.Journal of mathematical biology · 2023Article
- The tectonic complex regulates membrane protein composition in the photoreceptor cilium.Nature communications · 2023Article
- Absolute Quantification of Photoreceptor Outer Segment Proteins.Journal of proteome research · 2023Article
- Article
- Bicarbonate boosts flash response amplitude to augment absolute sensitivity and extend dynamic range in murine retinal rods.Frontiers in molecular neuroscience · 2023Article
- Generation of an RCVRN-eGFP Reporter hiPSC Line by CRISPR/Cas9 to Monitor Photoreceptor Cell Development and Facilitate the Cell Enrichment for Transplantation.Frontiers in cell and developmental biology · 2022Article
- Pepperberg plot: Modeling flash response saturation in retinal rods of mouse.Frontiers in molecular neuroscience · 2022Article
- Article
- Functional modulation of phosphodiesterase-6 by calcium in mouse rod photoreceptors.Scientific reports · 2021Article
- On the Wrong Track: Alterations of Ciliary Transport in Inherited Retinal Dystrophies.Frontiers in cell and developmental biology · 2021Review
- Phosphorylation at Serine 21 in G protein-coupled receptor kinase 1 (GRK1) is required for normal kinetics of dark adaption in rod but not cone photoreceptors.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- A Comparison of the Primary Sensory Neurons Used in Olfaction and Vision.Frontiers in cellular neuroscience · 2020Review
- Voltage-clamp recordings of light responses from wild-type and mutant mouse cone photoreceptors.The Journal of general physiology · 2019Article
- Rod Photoresponse Kinetics Limit Temporal Contrast Sensitivity in Mesopic Vision.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Elementary response triggered by transducin in retinal rods.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Investigating the CaScientific reports · 2018Article
- The PDE6 mutation in the rd10 retinal degeneration mouse model causes protein mislocalization and instability and promotes cell death through increased ion influx.The Journal of biological chemistry · 2018Article
- Role of recoverin in rod photoreceptor light adaptation.The Journal of physiology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Light isomerizes 11-cis-retinal in a retinal rod and produces an active form of rhodopsin (Rh*) that binds to the G-protein transducin and activates the phototransduction cascade. Rh* is turned off by phosphorylation by rhodopsin kinase [G-protein-coupled receptor kinase 1 (GRK1)] and subsequent binding of arrestin. To evaluate the role of GRK1 in rod light response decay, we have generated the transgenic mouse RKS561L in which GRK1, which is normally present at only 2-3% of rhodopsin, is overexpressed by ∼12-fold. Overexpression of GRK1 increases the rate of Rh* phosphorylation and reduces the exponential decay constant of the response (τ(REC)) and the limiting time constant (τ(D)) both by ∼30%; these decreases are highly significant. Similar decreases are produced in Rv(-/-) rods, in which the GRK1-binding protein recoverin has been genetically deleted. These changes in response decay are produced by acceleration of light-activated phosphodiesterase (PDE*) decay rather than Rh* decay, because light-activated PDE* decay remains rate limiting for response decay in both RKS561L and Rv(-/-) rods. A model incorporating an effect of GRK1 on light-activated PDE* decay rate can satisfactorily account for the changes in response amplitude and waveform. Modulation of response decay in background light is nearly eliminated by deletion of recoverin. Our experiments indicate that rhodopsin kinase and recoverin, in addition to their well-known role in regulating the turning off of Rh*, can also modulate the decay of light-activated PDE*, and the effects of these proteins on light-activated PDE* decay may be responsible for the quickening of response recovery in background light.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.