Literature DB >> 32307445

Resolving the dark matter of ABCA4 for 1054 Stargardt disease probands through integrated genomics and transcriptomics.

Claire-Marie Dhaenens1,2, Frans P M Cremers3,4, Mubeen Khan1,5, Stéphanie S Cornelis1,5, Marta Del Pozo-Valero1,6, Laura Whelan7, Esmee H Runhart5,8, Ketan Mishra1,5, Femke Bults1, Yahya AlSwaiti9, Alaa AlTalbishi9, Elfride De Baere10, Sandro Banfi11, Eyal Banin12, Miriam Bauwens10, Tamar Ben-Yosef13, Camiel J F Boon14,15, L Ingeborgh van den Born16,17, Sabine Defoort18, Aurore Devos2, Adrian Dockery7, Lubica Dudakova19, Ana Fakin20, G Jane Farrar7, Juliana Maria Ferraz Sallum21,22, Kaoru Fujinami23,24,25,26, Christian Gilissen1,27, Damjan Glavač28, Michael B Gorin29,30, Jacquie Greenberg31, Takaaki Hayashi32, Ymkje M Hettinga33, Alexander Hoischen1, Carel B Hoyng5,8, Karsten Hufendiek34, Herbert Jägle35, Smaragda Kamakari36, Marianthi Karali11, Ulrich Kellner37,38, Caroline C W Klaver8,39,40, Bohdan Kousal19,41, Tina M Lamey42,43, Ian M MacDonald44, Anna Matynia29,30, Terri L McLaren42,43, Marcela D Mena45, Isabelle Meunier46, Rianne Miller1, Hadas Newman47,48, Buhle Ntozini31, Monika Oldak49, Marc Pieterse1, Osvaldo L Podhajcer45, Bernard Puech18, Raj Ramesar31, Klaus Rüther50, Manar Salameh9, Mariana Vallim Salles21,22, Dror Sharon12, Francesca Simonelli51, Georg Spital52, Marloes Steehouwer1, Jacek P Szaflik53, Jennifer A Thompson43, Caroline Thuillier54, Anna M Tracewska55, Martine van Zweeden1, Andrea L Vincent56,57, Xavier Zanlonghi58, Petra Liskova19,41, Heidi Stöhr59, John N De Roach42,43, Carmen Ayuso6, Lisa Roberts31, Bernhard H F Weber59.   

Abstract

PURPOSE: Missing heritability in human diseases represents a major challenge, and this is particularly true for ABCA4-associated Stargardt disease (STGD1). We aimed to elucidate the genomic and transcriptomic variation in 1054 unsolved STGD and STGD-like probands.
METHODS: Sequencing of the complete 128-kb ABCA4 gene was performed using single-molecule molecular inversion probes (smMIPs), based on a semiautomated and cost-effective method. Structural variants (SVs) were identified using relative read coverage analyses and putative splice defects were studied using in vitro assays.
RESULTS: In 448 biallelic probands 14 known and 13 novel deep-intronic variants were found, resulting in pseudoexon (PE) insertions or exon elongations in 105 alleles. Intriguingly, intron 13 variants c.1938-621G>A and c.1938-514G>A resulted in dual PE insertions consisting of the same upstream, but different downstream PEs. The intron 44 variant c.6148-84A>T resulted in two PE insertions and flanking exon deletions. Eleven distinct large deletions were found, two of which contained small inverted segments. Uniparental isodisomy of chromosome 1 was identified in one proband.
CONCLUSION: Deep sequencing of ABCA4 and midigene-based splice assays allowed the identification of SVs and causal deep-intronic variants in 25% of biallelic STGD1 cases, which represents a model study that can be applied to other inherited diseases.

Entities:  

Keywords:  ABCA4; Stargardt disease; deep-intronic variants; smMIPs; structural variants

Mesh:

Substances:

Year:  2020        PMID: 32307445     DOI: 10.1038/s41436-020-0787-4

Source DB:  PubMed          Journal:  Genet Med        ISSN: 1098-3600            Impact factor:   8.822


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