ArticleThe Journal of biological chemistry2010
Mutations of the opsin gene (Y102H and I307N) lead to light-induced degeneration of photoreceptors and constitutive activation of phototransduction in mice.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 44 citations in OpenAlex.
- Tracking Systemic and Ocular Vitamin A.Cells · 2026Article
- Preventing light-induced toxicity in a new mouse model of sector retinitis pigmentosa caused by Rhodopsin M39R variant.Cell death discovery · 2025Article
- Identifying genetic determinants of outer retinal function in mice using a large-scale gene-targeted screen.PLoS genetics · 2025Article
- Light as a Mediator of Acute and Chronic Retina Degeneration.Advances in experimental medicine and biology · 2025Review
- Synchronized Photoactivation of T4K Rhodopsin Causes a Chromophore-Dependent Retinal Degeneration That Is Moderated by Interaction with Phototransduction Cascade Components.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Voluntary exercise preserves visual function and reduces inflammatory response in an adult mouse model of autosomal dominant retinitis pigmentosa.Scientific reports · 2024Article
- Fundus autofluorescence imaging using red excitation light.Scientific reports · 2023Article
- Dark-reared rd10 mice experience rapid photoreceptor degeneration with short exposure to room-light during in vivo retinal imaging.Experimental eye research · 2022Article
- New insights into the molecular mechanism of rhodopsin retinitis pigmentosa from the biochemical and functional characterization of G90V, Y102H and I307N mutations.Cellular and molecular life sciences : CMLS · 2022Article
- Nutraceutical Molecules Slow Down Retinal Degeneration, in Tvrm4 Mice a Model of Retinitis Pigmentosa, by Genetic Modulation of Anti-oxidant Pathway.Frontiers in neuroscience · 2022Article
- Gene Therapy for Rhodopsin-associated Autosomal Dominant Retinitis Pigmentosa.International ophthalmology clinics · 2021Article
- Retinal Pigment Epithelium Remodeling in Mouse Models of Retinitis Pigmentosa.International journal of molecular sciences · 2021Article
- Effect of Sodium Valproate on the Conformational Stability of the Visual G Protein-Coupled Receptor Rhodopsin.Molecules (Basel, Switzerland) · 2021Article
- Automated segmentation and analysis of retinal microglia within ImageJ.Experimental eye research · 2021Article
- Sectoral activation of glia in an inducible mouse model of autosomal dominant retinitis pigmentosa.Scientific reports · 2020Article
- Inner retinal preservation in the photoinducible I307N rhodopsin mutant mouse, a model of autosomal dominant retinitis pigmentosa.The Journal of comparative neurology · 2020Article
- Review
- Lessons learned from quantitative fundus autofluorescence.Progress in retinal and eye research · 2020Review
- Myriocin Effect on Tvrm4 Retina, an Autosomal Dominant Pattern of Retinitis Pigmentosa.Frontiers in neuroscience · 2020Article
- Aberrant RNA splicing is the major pathogenic effect in a knock-in mouse model of the dominantly inherited c.1430A>G human RPE65 mutation.Human mutation · 2019Article
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
Mutations in the Rhodopsin (Rho) gene can lead to autosomal dominant retinitis pigmentosa (RP) in humans. Transgenic mouse models with mutations in Rho have been developed to study the disease. However, it is difficult to know the source of the photoreceptor (PR) degeneration in these transgenic models because overexpression of wild type (WT) Rho alone can lead to PR degeneration. Here, we report two chemically mutagenized mouse models carrying point mutations in Rho (Tvrm1 with an Y102H mutation and Tvrm4 with an I307N mutation). Both mutants express normal levels of rhodopsin that localize to the PR outer segments and do not exhibit PR degeneration when raised in ambient mouse room lighting; however, severe PR degeneration is observed after short exposures to bright light. Both mutations also cause a delay in recovery following bleaching. This defect might be due to a slower rate of chromophore binding by the mutant opsins compared with the WT form, and an increased rate of transducin activation by the unbound mutant opsins, which leads to a constitutive activation of the phototransduction cascade as revealed by in vitro biochemical assays. The mutant-free opsins produced by the respective mutant Rho genes appear to be more toxic to PRs, as Tvrm1 and Tvrm4 mutants lacking the 11-cis chromophore degenerate faster than mice expressing WT opsin that also lack the chromophore. Because of their phenotypic similarity to humans with B1 Rho mutations, these mutants will be important tools in examining mechanisms underlying Rho-induced RP and for testing therapeutic strategies.
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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.