LRRTM4-C538Y novel gene mutation is associated with hereditary macular degeneration with novel dysfunction of ON-type bipolar cells.
Yuichi KawamuraAkiko SugaTakuro FujimakiKazutoshi YoshitakeKazushige TsunodaAkira MurakamiTakeshi IwataPublished in: Journal of human genetics (2018)
The macula is a unique structure in higher primates, where cone and rod photoreceptors show highest density in the fovea and the surrounding area, respectively. The hereditary macular dystrophies represent a heterozygous group of rare disorders characterized by central visual loss and atrophy of the macula and surrounding retina. Here we report an atypical absence of ON-type bipolar cell response in a Japanese patient with autosomal dominant macular dystrophy (adMD). To identify a causal genetic mutation for the adMD, we performed whole-exome sequencing (WES) on four affected and four-non affected members of the family for three generations, and identified a novel p.C538Y mutation in a post-synaptic gene, LRRTM4. WES analysis revealed seven rare genetic variations in patients. We further referred to our in-house WES data from 1360 families with inherited retinal diseases, and found that only p.C538Y mutation in LRRTM4 was associated with adMD-affected patients. Combinatorial filtration using public database of single-nucleotide polymorphism frequency and genotype-phenotype annotated database identified novel mutation in atypical adMD.
Keyphrases
- transcription factor
- optical coherence tomography
- diabetic retinopathy
- end stage renal disease
- newly diagnosed
- ejection fraction
- chronic kidney disease
- prognostic factors
- genome wide
- single cell
- induced apoptosis
- emergency department
- stem cells
- patient reported outcomes
- copy number
- gene expression
- mesenchymal stem cells
- case report
- artificial intelligence
- electronic health record
- adverse drug
- age related macular degeneration
- bone marrow
- optic nerve
- cell cycle arrest