通过外显子组数据再分析检测到的致病隐性变异可显著提高朱伯综合征的诊断率。

IF 3.7 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Fulvio D'Abrusco, Valentina Serpieri, Cecilia Maria Taccagni, Jessica Garau, Luca Cattaneo, Monica Boggioni, Simone Gana, Roberta Battini, Enrico Bertini, Ginevra Zanni, Eugen Boltshauser, Renato Borgatti, Romina Romaniello, Sabrina Signorini, Vincenzo Leuzzi, Caterina Caputi, Filippo Manti, Stefano D'Arrigo, Arianna De Laurentiis, Claudio Graziano, Johannes R Lemke, Federica Morelli, Danijela Petković Ramadža, Fabio Sirchia, Elisa Giorgio, Enza Maria Valente
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引用次数: 0

摘要

朱伯综合征(JS)是一种遗传异质性神经发育性纤毛症。尽管进行了外显子组测序(ES),但仍有一些患者未被确诊。本研究旨在通过有针对性的 ES 再分析发现隐性变异,从而提高诊断率。我们首先关注了 26 例患者,这些患者的 ES 只发现了一个 JS 基因中的杂合致病编码变异。我们重新分析了原始 ES 数据,搜索拷贝数变异(CNV)和影响剪接的内含子变异。我们通过实时 PCR 或染色体芯片验证了 CNV,通过 RT-PCR 或迷你基因验证了剪接变异。然后在另外 44 个 ES 阴性的 JS 中搜索隐性变异。我们在 26 名儿童中的 14 人(54%)中发现了隐性 "二次命中",在 44 人中的 3 人(7%)中发现了双倍拷贝隐性变异,在 70 人中的 17 人中得出了明确诊断(总体诊断增益为 24%)。我们的研究表明,CNVs 和内含子剪接变异是 JS 常见的突变机制;更重要的是,我们证明,只需对现有的 ES 数据进行集中再分析,就能发现很大一部分此类变异,尤其是在以前发现携带 KIAA0586、CC2D2A 和 CPLANE1 基因杂合编码变异的患者中,诊断率显著提高。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pathogenic cryptic variants detectable through exome data reanalysis significantly increase the diagnostic yield in Joubert syndrome.

Joubert syndrome (JS) is a genetically heterogeneous neurodevelopmental ciliopathy. Despite exome sequencing (ES), several patients remain undiagnosed. This study aims to increase the diagnostic yield by uncovering cryptic variants through targeted ES reanalysis. We first focused on 26 patients in whom ES only disclosed heterozygous pathogenic coding variants in a JS gene. We reanalyzed raw ES data searching for copy number variants (CNVs) and intronic variants affecting splicing. We validated CNVs through real-time PCR or chromosomal microarray, and splicing variants through RT-PCR or minigenes. Cryptic variants were then searched in additional 44 ES-negative JS individuals. We identified cryptic "second hits" in 14 of 26 children (54%) and biallelic cryptic variants in 3 of 44 (7%), reaching a definite diagnosis in 17 of 70 (overall diagnostic gain 24%). We show that CNVs and intronic splicing variants are a common mutational mechanism in JS; more importantly, we demonstrate that a significant proportion of such variants can be disclosed simply through a focused reanalysis of available ES data, with a significantly increase of the diagnostic yield especially among patients previously found to carry heterozygous coding variants in the KIAA0586, CC2D2A and CPLANE1 genes.

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来源期刊
European Journal of Human Genetics
European Journal of Human Genetics 生物-生化与分子生物学
CiteScore
9.90
自引率
5.80%
发文量
216
审稿时长
2 months
期刊介绍: The European Journal of Human Genetics is the official journal of the European Society of Human Genetics, publishing high-quality, original research papers, short reports and reviews in the rapidly expanding field of human genetics and genomics. It covers molecular, clinical and cytogenetics, interfacing between advanced biomedical research and the clinician, and bridging the great diversity of facilities, resources and viewpoints in the genetics community. Key areas include: -Monogenic and multifactorial disorders -Development and malformation -Hereditary cancer -Medical Genomics -Gene mapping and functional studies -Genotype-phenotype correlations -Genetic variation and genome diversity -Statistical and computational genetics -Bioinformatics -Advances in diagnostics -Therapy and prevention -Animal models -Genetic services -Community genetics
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