D'Abrusco Fulvio, Serpieri Valentina, Taccagni Cecilia Maria, Garau Jessica, Cattaneo Luca, Boggioni Monica, Gana Simone, Battini Roberta, Bertini Enrico, Zanni Ginevra, Boltshauser Eugen, Borgatti Renato, Romaniello Romina, Signorini Sabrina, Leuzzi Vincenzo, Caputi Caterina, Manti Filippo, D'Arrigo Stefano, De Laurentiis Arianna, Graziano Claudio, Lemke Johannes R, Morelli Federica, Petković Ramadža Danijela, Sirchia Fabio, Giorgio Elisa, Valente Enza Maria
Department of Molecular Medicine, University of Pavia, Pavia, Italy.
Neurogenetics Research Centre, IRCCS Mondino Foundation, Pavia, Italy.
Eur J Hum Genet. 2025 Jan;33(1):72-79. doi: 10.1038/s41431-024-01703-x. Epub 2024 Oct 11.
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.
乔伯特综合征(JS)是一种具有遗传异质性的神经发育性纤毛病。尽管进行了外显子组测序(ES),仍有部分患者未得到诊断。本研究旨在通过对靶向ES重新分析来发现隐匿性变异,从而提高诊断率。我们首先聚焦于26例患者,这些患者的ES仅揭示了JS基因中的杂合致病性编码变异。我们重新分析原始ES数据,以寻找拷贝数变异(CNV)和影响剪接的内含子变异。我们通过实时PCR或染色体微阵列验证CNV,通过RT-PCR或小基因验证剪接变异。然后在另外44例ES阴性的JS个体中搜索隐匿性变异。我们在26名儿童中的14名(54%)中发现了隐匿性“二次打击”,在44名中的3名(7%)中发现了双等位基因隐匿性变异,在70名患者中有17名得到了明确诊断(总体诊断率提高了24%)。我们表明,CNV和内含子剪接变异是JS中常见的突变机制;更重要的是,我们证明,通过对现有ES数据进行重点重新分析,可简单地揭示相当一部分此类变异,特别是在先前发现携带KIAA0586、CC2D2A和CPLANE1基因杂合编码变异的患者中,诊断率显著提高。