Hassan Mohamed Ahamed, Shah Aftab Ali, Szmida Elzbieta, Smigiel Robert, Sasiadek Maria M, Pfister Markus, Blin Nikolaus, Bress Andreas
Division of Molecular Genetics, University of Tuebingen, Tuebingen, Germany.
J Appl Genet. 2015 Aug;56(3):311-6. doi: 10.1007/s13353-014-0263-4. Epub 2015 Jan 6.
After excluding frequent mutations in common genes like GJB2, SLC26A4 and MT-RNR1 by straightforward Sanger sequencing in about 20 Polish families with hearing impairment, new and possibly pathogenic mutations were searched for by next-generation sequencing (NGS) screening using a specialised panel including more than 80 genes connected with hearing disorders. Due to high rates of false-positive pathogen predictions for newly discovered single-nucleotide polymorphisms (SNPs), different prediction models were combined to enhance the prediction power. In one family with a record of over four generations, II,3 and II,4 were suspected of hearing impairment without medical records. A male person (III,2) displayed hearing loss of 40 dB hearing level (HL) and his two sons, IV,1 and IV,2, were both affected; one with 90 dB HL and the other with 40 dB HL. Here, one heterozygous, non-synonymous variant was detected, with the SNP causing an amino acid substitution in TMC1 (transmembrane channel-like 1), a gene reported with many mutations in DFNA36 and DFNB7/11 (OMIM #606705 and #600974, respectively). Until now, the substitution p.S320R has not been described in any database. Instead of the significance of this mutation by bioinformatics tools, we confirmed the genotype-phenotype co-segregation in family members. The involvement of TMC1 in hereditary hearing impairment has not been observed in the Polish population so far.
在对约20个患有听力障碍的波兰家庭进行直接桑格测序以排除常见基因如GJB2、SLC26A4和MT-RNR1中的常见突变后,通过使用包含80多个与听力障碍相关基因的专门面板进行下一代测序(NGS)筛选来寻找新的可能致病突变。由于新发现的单核苷酸多态性(SNP)的假阳性病原体预测率较高,因此将不同的预测模型结合起来以提高预测能力。在一个有四代以上记录的家庭中,II,3和II,4疑似有听力障碍但无病历记录。一名男性(III,2)表现出40分贝听力水平(HL)的听力损失,他的两个儿子IV,1和IV,2均受影响;一个为90分贝HL,另一个为40分贝HL。在此,检测到一个杂合的非同义变体,该SNP在TMC1(跨膜通道样1)中导致氨基酸替代,TMC1基因在DFNA36和DFNB7/11(分别为OMIM #606705和#600974)中有许多突变报道。到目前为止,任何数据库中都未描述过p.S320R替代。我们没有通过生物信息学工具确定该突变的意义,而是在家庭成员中证实了基因型-表型共分离。迄今为止,在波兰人群中尚未观察到TMC1与遗传性听力障碍有关。