Kim Ye-Ri, Lee Byeonghyeon, Park Hong-Joon, Kwon Tae-Jun, Kim Un-Kyung
Department of Immunology, School of Medicine, Kyungpook National University, Daegu, Republic of Korea.
Advanced Bio-resource Research Center, Kyungpook National University, Daegu, Republic of Korea.
Genes Genomics. 2025 Jun 26. doi: 10.1007/s13258-025-01653-8.
Hereditary hearing loss (HHL) exhibits considerable genetic heterogeneity. Among the known causative genes, MYO7A is frequently linked to autosomal recessive non-syndromic hearing loss (ARNSHL), contributing to auditory dysfunction through impaired inner ear cellular mechanics.
This study aimed to identify the genetic cause of ARNSHL in a Korean family (SR-323) and to assess the pathogenicity of candidate MYO7A variants.
Whole-exome sequencing (WES) was performed on five family members (two affected individuals and three unaffected relatives). Variant filtering, co-segregation analysis, and Sanger sequencing validation were conducted to identify candidate mutations. Conservation analysis across vertebrate species and in silico pathogenicity predictions were used to evaluate the biological impact of the variants. Additionally, 100 unrelated normal-hearing Korean individuals were screened to determine the frequency of the variant in the general population.
Two MYO7A variants, c.4501G > A (p.Val1501Met) and c.6070 C > T (p.Arg2024Stop), were identified in affected individuals in a compound heterozygous state. Unaffected family members carried only one heterozygous variant. Both amino acid residues were highly conserved across seven vertebrate species. In silico analyses predicted p.Val1501Met to be pathogenic, while c.6070 C > T was previously classified as likely pathogenic. These variants were absent in the normal-hearing cohort, and only individuals with both variants exhibited hearing loss, supporting a compound heterozygous inheritance.
Compound heterozygosity of the MYO7A variants c.4501G > A and c.6070 C > T likely underlies the ARNSHL phenotype in the SR-323 family. These findings expand the known mutational spectrum of MYO7A and highlight the importance of genetic screening in hereditary hearing loss within the Korean population.
遗传性听力损失(HHL)表现出相当大的遗传异质性。在已知的致病基因中,MYO7A常与常染色体隐性非综合征性听力损失(ARNSHL)相关,通过内耳细胞力学受损导致听觉功能障碍。
本研究旨在确定一个韩国家庭(SR - 323)中ARNSHL的遗传病因,并评估候选MYO7A变体的致病性。
对五名家庭成员(两名受影响个体和三名未受影响亲属)进行全外显子组测序(WES)。进行变体筛选、共分离分析和桑格测序验证以鉴定候选突变。通过跨脊椎动物物种的保守性分析和计算机致病性预测来评估变体的生物学影响。此外,对100名听力正常的非相关韩国个体进行筛查,以确定该变体在一般人群中的频率。
在受影响个体中鉴定出两个处于复合杂合状态的MYO7A变体,即c.4501G>A(p.Val1501Met)和c.6070 C>T(p.Arg2024Stop)。未受影响的家庭成员仅携带一个杂合变体。这两个氨基酸残基在七种脊椎动物物种中高度保守。计算机分析预测p.Val1501Met具有致病性,而c.6070 C>T先前被归类为可能具有致病性。这些变体在听力正常的队列中不存在,并且只有同时携带这两个变体的个体表现出听力损失,支持复合杂合遗传。
MYO7A变体c.4501G>A和c.6070 C>T的复合杂合性可能是SR - 323家庭中ARNSHL表型的基础。这些发现扩展了已知的MYO7A突变谱,并突出了韩国人群中遗传性听力损失基因筛查的重要性。