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半合子缺失所揭示的变异的发现。

Discovery of variants unmasked by hemizygous deletions.

机构信息

Department of Medical Genetics, University Medical Center Utrecht, Utrecht, The Netherlands.

出版信息

Eur J Hum Genet. 2012 Jul;20(7):748-53. doi: 10.1038/ejhg.2011.263. Epub 2012 Jan 18.

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.

摘要

基于阵列的全基因组片段性非整倍体筛查可检测到新发和遗传拷贝数变异 (CNV)。在散发性患者中,新发 CNV 被解释为潜在的致病性。然而,如果从健康父母那里遗传的缺失与从另一个健康父母那里遗传的突变的第二个等位基因重叠,则可能是致病性的。为了检测此类事件,我们对 20 名患者(1.53Mb 捕获足迹)的独特半合缺失区域内所有基因的整个编码序列进行了多重富集和下一代测序。在所检测到的 703 个非同义单核苷酸变异 (SNV) 中,有 8 个代表因半合缺失而暴露的变异。虽然遗传模式、Grantham 矩阵评分、进化保守性和生物信息学预测的评估并未一致表明这些变异具有致病性,但如果没有功能验证,就无法得出明确的结论。然而,在一名患有严重智力迟钝、无言语、小头畸形、唇腭裂和双侧听力损失的患者中,我们发现了另一个较小的缺失,从另一个健康的父母那里遗传,导致高度保守的热休克因子结合蛋白 1 (HSBP1) 基因的两个等位基因丢失。可以想象,遗传缺失可能会揭示罕见的致病性变异,这些变异可能通过隐性基因作用模式产生表型影响。

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