American journal of human genetics · 2009
Mutations in TRPM1 are a common cause of complete congenital stationary night blindness.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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van Genderen Maria M, Bijveld Mieke M C, Claassen Yvonne B, Florijn Ralph J, Pearring Jillian N, Meire Francoise M, McCall Maureen A, Riemslag Frans C C, Gregg Ronald G, Bergen Arthur A B, Kamermans Maarten
Аннотация
Congenital stationary night blindness (CSNB) is a clinically and genetically heterogeneous group of retinal disorders characterized by nonprogressive impaired night vision and variable decreased visual acuity. We report here that six out of eight female probands with autosomal-recessive complete CSNB (cCSNB) had mutations in TRPM1, a retinal transient receptor potential (TRP) cation channel gene. These data suggest that TRMP1 mutations are a major cause of autosomal-recessive CSNB in individuals of European ancestry. We localized TRPM1 in human retina to the ON bipolar cell dendrites in the outer plexifom layer. Our results suggest that in humans, TRPM1 is the channel gated by the mGluR6 (GRM6) signaling cascade, which results in the light-evoked response of ON bipolar cells. Finally, we showed that detailed electroretinography is an effective way to discriminate among patients with mutations in either TRPM1 or GRM6, another autosomal-recessive cCSNB disease gene. These results add to the growing importance of the diverse group of TRP channels in human disease and also provide new insights into retinal circuitry.
Предметные рубрики MeSH
Amino Acid SequenceCase-Control StudiesChromosome DeletionCohort StudiesElectroretinographyExonsFemaleGenes, RecessiveHeterozygoteHomozygoteHumansModels, BiologicalMolecular Sequence DataMutationMutation, MissenseNight BlindnessNuclear FamilyRetinal Rod Photoreceptor CellsSignal TransductionTRPM Cation ChannelsWhite People