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Intron Mutations and Early Transcription Termination in Duchenne and Becker muscular dystrophy
Journal article   Open access   Peer reviewed

Intron Mutations and Early Transcription Termination in Duchenne and Becker muscular dystrophy

Megan A Waldrop, Steven A Moore, Katherine D Mathews, Benjamin W Darbro, Livja Medne, Richard Finkel, Anne M Connolly, Thomas O Crawford, Daniel Drachman, Nicolas Wein, …
Human mutation, Vol.43(4), pp.511-528
02/14/2022
DOI: 10.1002/humu.24343
PMCID: PMC9901284
PMID: 35165973
url
https://doi.org/10.1002/humu.24343View
Published (Version of record) Open Access

Abstract

DMD pathogenic variants for Duchenne and Becker muscular dystrophy are detectable with high sensitivity by standard clinical exome analyses of genomic DNA. However, up to 7% of DMD mutations are deep intronic and analysis of muscle-derived RNA is an important diagnostic step for patients who have negative genomic testing but abnormal dystrophin expression in muscle. In this study, muscle biopsies were evaluated from 19 patients with clinical features of a dystrophinopathy, but negative clinical DMD mutation analysis. Reverse transcription PCR (RT-PCR) or high-throughput RNA sequencing (RNA-Seq) methods identified 19 mutations with one of three pathogenic pseudoexon types: deep intronic point mutations, deletions or insertions, and translocations. In association with point mutations creating intronic splice acceptor sites, we observed the first examples of DMD pseudo 3'-terminal exon mutations causing high efficiency transcription termination within introns. This connection between splicing and premature transcription termination is reminiscent of U1 snRNP-mediating telescripting in sustaining RNA polymerase II elongation across large genes, such as DMD. We propose a novel classification of three distinct types of mutations identifiable by muscle RNA analysis, each of which differ in potential treatment approaches. Recognition and appropriate characterization may lead to therapies directed toward full-length dystrophin expression for some patients. This article is protected by copyright. All rights reserved.
Becker muscular dystrophy deep intronic telescripting Duchenne muscular dystrophy transcription termination pseudoexon

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