Department of Otorhinolaryngology-Head and Neck Surgery, Faculty of Medicine and University Hospital, Comenius University, Bratislava, Slovakia.
DIABGENE Laboratory, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovakia.
Sci Rep. 2021 Nov 18;11(1):22488. doi: 10.1038/s41598-021-01876-1.
The genetic heterogeneity of sensorineural hearing loss (SNHL) is a major hurdle to the detection of disease-causing variants. We aimed to identify underlying causal genes associated with mid-frequency hearing loss (HL), which contributes to less than about 1% of SNHL cases, by whole exome sequencing (WES). Thirty families segregating mid-frequency SNHL, in whom biallelic GJB2 mutations had been previously excluded, were selected from among 851 families in our DNA repository of SNHL. DNA samples from the probands were subjected to WES analysis and searched for candidate variants associated with SNHL. We were able to identify the genetic aetiology in six probands (20%). In total, we found three pathogenic and three likely pathogenic variants in four genes (COL4A5, OTOGL, TECTA, TMPRSS3). One more proband was a compound heterozygote for a pathogenic variant and a variant of uncertain significance (VUS) in MYO15A gene. To date, MYO15A and TMPRSS3 have not yet been described in association with mid-frequency SNHL. In eight additional probands, eight candidate VUS variants were detected in five genes (DIAPH1, MYO7A, TECTA, TMC1, TSPEAR). Seven of these 16 variants have not yet been published or mentioned in the available databases. The most prevalent gene was TECTA, identified in 23% of all tested families. Furthermore, we confirmed the hypothesis that a substantive portion of cases with this conspicuous audiogram shape is a consequence of a genetic disorder.
感音神经性听力损失(SNHL)的遗传异质性是发现致病变异的主要障碍。我们旨在通过全外显子组测序(WES)发现与中频率听力损失(HL)相关的潜在致病基因,中频率听力损失导致的 SNHL 病例不到 1%。从我们的 SNHL DNA 库中的 851 个家族中,选择了 30 个有中频率 SNHL 遗传的家族,这些家族中先前已排除了双等位基因 GJB2 突变。对先证者的 DNA 样本进行 WES 分析,并寻找与 SNHL 相关的候选变异。我们能够在 6 个先证者(20%)中确定遗传病因。总共在 4 个基因(COL4A5、OTOGL、TECTA、TMPRSS3)中发现了 3 个致病性和 3 个可能致病性的变体。还有一个先证者是 MYO15A 基因的致病性变体和意义不明的变体(VUS)的复合杂合子。迄今为止,MYO15A 和 TMPRSS3 尚未与中频率 SNHL 相关联。在另外 8 个先证者中,在 5 个基因(DIAPH1、MYO7A、TECTA、TMC1、TSPEAR)中检测到 8 个候选 VUS 变体。这 16 个变体中有 7 个尚未在可用数据库中公布或提及。最常见的基因是 TECTA,在所有测试的家族中占 23%。此外,我们证实了一个假设,即这种明显的听力图形状的大部分病例是遗传疾病的结果。