ArticleVisual neuroscience2015
Identification of a new mutant allele, Grm6(nob7), for complete congenital stationary night blindness.
Article in Visual neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Novel Grm6 Variant in a no b-wave (nob) Mouse Model: Phenotype Characterization and Gene Therapy.Investigative ophthalmology & visual science · 2025Article
- Gene therapy shines light on congenital stationary night blindness for future cures.Journal of translational medicine · 2025Review
- Compound heterozygous mutations inHeliyon · 2024Article
- AInternational journal of molecular sciences · 2024Article
- Mice LackingInternational journal of molecular sciences · 2022Article
- Functional regulation of an outer retina hyporeflective band on optical coherence tomography images.Scientific reports · 2021Article
- A New Mouse Model for Complete Congenital Stationary Night Blindness Due toInternational journal of molecular sciences · 2021Article
- Restoration of mGluR6 Localization Following AAV-Mediated Delivery in a Mouse Model of Congenital Stationary Night Blindness.Investigative ophthalmology & visual science · 2021Article
- Molecular mechanisms underlying selective synapse formation of vertebrate retinal photoreceptor cells.Cellular and molecular life sciences : CMLS · 2020Review
- Genome-wide association study and whole-genome sequencing identify a deletion in LRIT3 associated with canine congenital stationary night blindness.Scientific reports · 2019Article
- Reduced expression of theMolecular vision · 2019Article
- LRIT1 Modulates Adaptive Changes in Synaptic Communication of Cone Photoreceptors.Cell reports · 2018Article
- A missense mutation inJournal of neurophysiology · 2017Article
- LRIT3 Differentially Affects Connectivity and Synaptic Transmission of Cones to ON- and OFF-Bipolar Cells.Investigative ophthalmology & visual science · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Electroretinogram (ERG) studies identified a new mouse line with a normal a-wave but lacking the b-wave component. The ERG phenotype of this new allele, nob7, matched closely that of mouse mutants for Grm6, Lrit3, Trpm1, and Nyx, which encode for proteins expressed in depolarizing bipolar cells (DBCs). To identify the underlying mutation, we first crossed nob7 mice with Grm6 nob3 mutants and measured the ERGs in offspring. All the offspring lacked the b-wave, indicating that nob7 is a new allele for Grm6: Grm6 nob7 . Sequence analyses of Grm6 nob7 cDNAs identified a 28 base pair insertion between exons 8 and 9, which would result in a frameshift mutation in the open reading frame that encodes the metabotropic glutamate receptor 6 (Grm6). Sequencing both the cDNA and genomic DNA from exon 8 and intron 8, respectively, from the Grm6 nob7 mouse revealed a G to A transition at the last position in exon 8. This mutation disrupts splicing and the normal exon 8 is extended by 28 base pairs, because splicing occurs 28 base pairs downstream at a cryptic splice donor. Consistent with the impact of the resulting frameshift mutation, there is a loss of mGluR6 protein (encoded by Grm6) from the dendritic tips of DBCs in the Grm6 nob7 retina. These results indicate that Grm6 nob7 is a new model of the complete form of congenital stationary night blindness, a human condition that has been linked to mutations of GRM6.
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Registered trials
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.