| Literature DB >> 22258528 |
Ron Hochstenbach1, Martin Poot, Isaac J Nijman, Ivo Renkens, Karen J Duran, Ruben Van't Slot, Ellen van Binsbergen, Bert van der Zwaag, Maartje J Vogel, Paulien A Terhal, Hans Kristian Ploos van Amstel, Wigard P Kloosterman, Edwin Cuppen.
Abstract
Array-based genome-wide segmental aneuploidy screening detects both de novo and inherited copy number variations (CNVs). In sporadic patients de novo CNVs are interpreted as potentially pathogenic. However, a deletion, transmitted from a healthy parent, may be pathogenic if it overlaps with a mutated second allele inherited from the other healthy parent. To detect such events, we performed multiplex enrichment and next-generation sequencing of the entire coding sequence of all genes within unique hemizygous deletion regions in 20 patients (1.53 Mb capture footprint). Out of the detected 703 non-synonymous single-nucleotide variants (SNVs), 8 represented variants being unmasked by a hemizygous deletion. Although evaluation of inheritance patterns, Grantham matrix scores, evolutionary conservation and bioinformatic predictions did not consistently indicate pathogenicity of these variants, no definitive conclusions can be drawn without functional validation. However, in one patient with severe mental retardation, lack of speech, microcephaly, cheilognathopalatoschisis and bilateral hearing loss, we discovered a second smaller deletion, inherited from the other healthy parent, resulting in loss of both alleles of the highly conserved heat shock factor binding protein 1 (HSBP1) gene. Conceivably, inherited deletions may unmask rare pathogenic variants that may exert a phenotypic impact through a recessive mode of gene action.Entities:
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Year: 2012 PMID: 22258528 PMCID: PMC3376260 DOI: 10.1038/ejhg.2011.263
Source DB: PubMed Journal: Eur J Hum Genet ISSN: 1018-4813 Impact factor: 4.246