| Literature DB >> 28251733 |
Kristin D Kernohan1,2, Laure Frésard3, Zachary Zappala3,4, Taila Hartley2, Kevin S Smith3, Justin Wagner2, Hongbin Xu5, Arran McBride2, Pierre R Bourque6, Care Rare Canada Consortium2, Steffany A L Bennett5, David A Dyment1,2, Kym M Boycott1,2, Stephen B Montgomery3,4, Jodi Warman Chardon1,2,6,7,8.
Abstract
At least 15% of the disease-causing mutations affect mRNA splicing. Many splicing mutations are missed in a clinical setting due to limitations of in silico prediction algorithms or their location in noncoding regions. Whole-transcriptome sequencing is a promising new tool to identify these mutations; however, it will be a challenge to obtain disease-relevant tissue for RNA. Here, we describe an individual with a sporadic atypical spinal muscular atrophy, in whom clinical DNA sequencing reported one pathogenic ASAH1 mutation (c.458A>G;p.Tyr153Cys). Transcriptome sequencing on patient leukocytes identified a highly significant and atypical ASAH1 isoform not explained by c.458A>G(p<10-16 ). Subsequent Sanger-sequencing identified the splice mutation responsible for the isoform (c.504A>C;p.Lys168Asn) and provided a molecular diagnosis of autosomal-recessive spinal muscular atrophy with progressive myoclonic epilepsy. Our findings demonstrate the utility of RNA sequencing from blood to identify splice-impacting disease mutations for nonhematological conditions, providing a diagnosis for these otherwise unsolved patients.Entities:
Keywords: ASAH1; next-generation sequencing; spinal muscular atrophy with progressive myoclonic epilepsy (SMA-PME); transcriptome sequencingzzm321990
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Year: 2017 PMID: 28251733 PMCID: PMC5889109 DOI: 10.1002/humu.23211
Source DB: PubMed Journal: Hum Mutat ISSN: 1059-7794 Impact factor: 4.878