NDLI: AMD-associated variants at the chromosome 10q26 locus and the stability of ARMS2 transcripts.

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AMD-associated variants at the chromosome 10q26 locus and the stability of ARMS2 transcripts.

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AMD-associated variants at the chromosome 10q26 locus and the stability of ARMS2 transcripts.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Court, Brenda L. Wang, Gaofeng Minor, Emily A. Dubovy, Sander
Description	Country affiliation: United States Author Affiliation: Minor EA ( John P. Hussman Institute for Human Genomics, Dr. John T. Macdonald Foundation, Department of Human Genetics, University of Miami Miller School of Medicine, Miami, Florida 33136, USA.)
Abstract	PURPOSE: To analyze the effect of variants including age-related macular degeneration (AMD)-associated combinative insertion/deletion polymorphism (indel) at 3'UTR of ARMS2 and possibly associated R38X on the stability of ARMS2 transcripts. METHODS: ARMS2 transcription from minigene vectors carrying different alleles at variants R38X and the indel were assessed in mouse embryonic fibroblasts (MEFs). Dual luciferase assays were applied to evaluate the effect of the indel on gene expression. RT-PCR and quantitative RT-PCR (qRT-PCR) were used to measure the two ARMS2 transcripts (isoform A and isoform B) in MEFs and human retina-RPE-choroid samples (n = 83). RESULTS: Allele X at variant R38X decreased exogenous ARMS2 transcripts in MEFs compared to allele R. In contrast, the indel did not change the level of exogenous ARMS2 transcripts. After blocking transcription by actinomycin D, R38X appeared to accelerate the degradation of ARMS2 transcripts, while the indel did not obviously affect the stability of ARMS2 transcripts compared to the wild-type (WT) allele. Dual luciferase assays further indicated that the indel did not influence gene expression. Quantitative RT-PCR results showed that there was no significant difference in two ARMS2 transcript splice isoforms among retina-RPE-choroid samples carrying different genotypes at variants R38X and the indel. CONCLUSIONS: Variant R38X, not the indel, decreases the stability of ARMS2 transcripts in vitro. However, genotypes at R38X and the indel do not obviously affect the level of ARMS2 transcripts in retina-RPE-choroid samples. These results suggest that variants R38X and the indel are less likely to play a pathogenic role in AMD by changing the level of ARMS2 transcripts.
ISSN	01460404
e-ISSN	15525783
Journal	Investigative Opthalmology & Visual Science
Issue Number	8
Volume Number	54
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2013-08-28
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Chromosomes, Human, Pair 10 Genetics Genetic Loci Genetic Predisposition To Disease Indel Mutation Macular Degeneration Polymorphism, Genetic Proteins Animals Choroid Metabolism Gene Expression Regulation Genetic Association Studies Mice Retina Reverse Transcriptase Polymerase Chain Reaction Research Support, Non-u.s. Gov't Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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