| Literature DB >> 24610719 |
Elisabeth Gillis1, Marlies Kempers, Simone Salemink, Janneke Timmermans, Emile C Cheriex, Sebastiaan C A M Bekkers, Erik Fransen, Christine E M De Die-Smulders, Bart L Loeys, Lut Van Laer.
Abstract
Marfan syndrome (MFS) is caused by mutations in the FBN1 (fibrillin-1) gene, but approximately 10% of MFS cases remain genetically unsolved. Here, we report a new FBN1 mutation in an MFS family that had remained negative after extensive molecular genomic DNA FBN1 testing, including denaturing high-performance liquid chromatography, Sanger sequencing, and multiplex ligation-dependent probe amplification. Linkage analysis in the family and cDNA sequencing of the proband revealed a deep intronic point mutation in intron 56 generating a new splice donor site. This mutation results in the integration of a 90-bp pseudo-exon between exons 56 and 57 containing a stop codon, causing nonsense-mediated mRNA decay. Although more than 90% of FBN1 mutations can be identified with regular molecular testing at the genomic level, deep intronic mutations will be missed and require cDNA sequencing or whole-genome sequencing.Entities:
Keywords: FBN1; Marfan syndrome; deep intronic mutation; pseudo-exon
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Year: 2014 PMID: 24610719 DOI: 10.1002/humu.22540
Source DB: PubMed Journal: Hum Mutat ISSN: 1059-7794 Impact factor: 4.878