ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Night blindness and the mechanism of constitutive signaling of mutant G90D rhodopsin.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. 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, 51 citations in OpenAlex.
- G-protein activation of the dark-state conformation of the visual G protein-coupled receptor rhodopsin by releasing critical structural constraints.Communications biology · 2026Article
- The physiology of dark adaptation: Progress and future directions.Progress in retinal and eye research · 2025Review
- The mechanism of genetically inherited night blindness.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Dark continuous noise from mutant G90D-rhodopsin predominantly underlies congenital stationary night blindness.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Disease modeling and pharmacological rescue of autosomal dominant retinitis pigmentosa associated witheLife · 2024Article
- Disease modeling and pharmacological rescue of autosomal dominant Retinitis Pigmentosa associated withmedRxiv : the preprint server for health sciences · 2023Article
- Rhodopsin-associated retinal dystrophy: Disease mechanisms and therapeutic strategies.Frontiers in neuroscience · 2023Review
- Regulation of retinal membrane guanylyl cyclase (RetGC) by negative calcium feedback and RD3 protein.Pflugers Archiv : European journal of physiology · 2021Review
- Structural aspects of rod opsin and their implication in genetic diseases.Pflugers Archiv : European journal of physiology · 2021Review
- Stationary and Progressive Phenotypes Caused by the p.G90D Mutation in Rhodopsin Gene.International journal of molecular sciences · 2021Article
- Differential Aggregation Properties of Mutant Human and Bovine Rhodopsin.Biochemistry · 2021Article
- Differential adaptations in rod outer segment disc membranes in different models of congenital stationary night blindness.Biochimica et biophysica acta. Biomembranes · 2020Article
- Dark noise and retinal degeneration from D190N-rhodopsin.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Light Dynamics of the Retinal-Disease-Relevant G90D Bovine Rhodopsin Mutant.Angewandte Chemie (International ed. in English) · 2020Article
- A Conserved Proline Hinge Mediates Helix Dynamics and Activation of Rhodopsin.Structure (London, England : 1993) · 2020Article
- Retinal degeneration in mice expressing the constitutively active G90D rhodopsin mutant.Human molecular genetics · 2020Article
- Characterizing variants of unknown significance in rhodopsin: A functional genomics approach.Human mutation · 2019Article
- Differentiating between Inactive and Active States of Rhodopsin by Atomic Force Microscopy in Native Membranes.Analytical chemistry · 2019Article
- Tauroursodeoxycholic acid binds to the G-protein site on light activated rhodopsin.Experimental eye research · 2018Article
- The molecular and cellular basis of rhodopsin retinitis pigmentosa reveals potential strategies for therapy.Progress in retinal and eye research · 2018Review
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The G90D rhodopsin mutation is known to produce congenital night blindness in humans. This mutation produces a similar condition in mice, because rods of animals heterozygous (D+) or homozygous (D+/+) for this mutation have decreased dark current and sensitivity, reduced Ca(2+), and accelerated values of tau(REC) and tau(D), similar to light-adapted wild-type (WT) rods. Our experiments indicate that G90D pigment activates the cascade, producing an equivalent background light of approximately 130 Rh* rod(-1) for D+ and 890 Rh* rod(-1) for D+/+. The active species of the G90D pigment could be unregenerated G90D opsin or G90D rhodopsin, either spontaneously activated (as Rh*) or in some other form. Addition of 11-cis-retinal in lipid vesicles, which produces regeneration of both WT and G90D opsin in intact rods and ROS membranes, had no effect on the waveform or sensitivity of dark-adapted G90D responses, indicating that the active species is not G90D opsin. The noise spectra of dark-adapted G90D and WT rods are similar, and the G90D noise variance is much less than of a WT rod exposed to background light of about the same intensity as the G90D equivalent light, indicating that Rh* is not the active species. We hypothesize that G90D rhodopsin undergoes spontaneous changes in molecular conformation which activate the transduction cascade with low gain. Our experiments provide the first indication that a mutant form of the rhodopsin molecule bound to its 11-cis-chromophore can stimulate the visual cascade spontaneously at a rate large enough to produce visual dysfunction.
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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.