Choi Hyun Seok, Kim Ah Reum, Kim Shin Hye, Choi Byung Yoon
Department of Otorhinolaryngology-Head and Neck Surgery, Seoul National University Bundang Hospital, College of Medicine, Seoul National University, 300 Gumi-dong, Bundang-gu, Seongnam, Kyunggi, 463-707, Korea.
Department of Otorhinolaryngology-Head and Neck Surgery, Seoul National University Hospital, Seoul, Korea.
Eur Arch Otorhinolaryngol. 2016 May;273(5):1123-9. doi: 10.1007/s00405-015-3661-2. Epub 2015 May 27.
The EYA4 gene encodes a 640-amino-acid protein that serves as a transcription factor. This protein contains a highly conserved Eya domain (eya-HR) and a variable domain (eya-VR). Mutations of this gene are known to cause postlingual and progressive sensorineural hearing loss, either as non-syndromic (DFNA10) or syndromic hearing loss, depending on the location of truncation of the mutant protein. Since our previous report, we have recruited 14 families segregating autosomal dominant moderate SNHL. A thorough medical history and physical examination including evaluation of heart problems ruled out any syndromic features in these families. Screening of EYA4 was performed by targeted exome sequencing of 134 known deafness genes (TES-134) from the probands. After basic filtering of the variants, we identified one proband who carried a novel truncation mutation, c.1194delT (p.Met401TrpfsX3) of EYA4, making the frequency of DFNA10 to be 7.14 % (1/14) in Koreans. The variant co-segregated perfectly with a slightly down-sloping, moderate degree of SNHL in the family (SH117), and was not detected in any of the 592 normal control chromosomes. This variant is likely to generate protein products that are truncated just downstream of the eya-VR domain. None of the three affected family members showed any syndromic features, including cardiac problems, which was compatible with a previous genotype-phenotype correlation. The identification of a novel EYA4 truncation mutation associated with DFNA10, rather than syndromic hearing loss, supports a previously reported genotype-phenotype correlation in this gene. Considering its detection rate, EYA4 mutations should be suspected in hereditary moderate hearing loss with a corresponding audiologic configuration, and a cardiac examination should be included in the initial evaluation.
EYA4基因编码一种640个氨基酸的蛋白质,该蛋白质作为一种转录因子。这种蛋白质包含一个高度保守的Eya结构域(eya-HR)和一个可变结构域(eya-VR)。已知该基因的突变会导致语言发育后进行性感音神经性听力损失,根据突变蛋白截断的位置,可表现为非综合征性(DFNA10)或综合征性听力损失。自我们之前的报告以来,我们招募了14个常染色体显性中度感音神经性听力损失的家系。通过全面的病史和体格检查,包括对心脏问题的评估,排除了这些家系中的任何综合征特征。通过对先证者的134个已知耳聋基因(TES-134)进行靶向外显子测序来筛查EYA4。在对变异进行基本筛选后,我们鉴定出一名携带EYA4基因新的截断突变c.1194delT(p.Met401TrpfsX3)的先证者,使得DFNA10在韩国人中的频率为7.14%(1/14)。该变异与家系(SH117)中轻度下降、中度感音神经性听力损失完全共分离,在592条正常对照染色体中均未检测到。该变异可能产生在eya-VR结构域下游截断的蛋白质产物。三名受影响的家庭成员均未表现出任何综合征特征,包括心脏问题,这与先前的基因型-表型相关性相符。与DFNA10而非综合征性听力损失相关的EYA4新截断突变的鉴定,支持了该基因先前报道的基因型-表型相关性。考虑到其检出率,对于具有相应听力学特征的遗传性中度听力损失,应怀疑EYA4突变,并且在初始评估中应包括心脏检查。