Paula I Buonfiglio, Carlos D Bruque, Lucía Salatino, Vanesa Lotersztein, Mariela Pace, Sofia Grinberg, Ana B Elgoyhen, Paola V Plazas, Viviana Dalamón
{"title":"在阿根廷舌后非综合征性听力损失家庭中发现的MYO6新变异的计算机和体内分析","authors":"Paula I Buonfiglio, Carlos D Bruque, Lucía Salatino, Vanesa Lotersztein, Mariela Pace, Sofia Grinberg, Ana B Elgoyhen, Paola V Plazas, Viviana Dalamón","doi":"10.1093/nargab/lqae162","DOIUrl":null,"url":null,"abstract":"<p><p>Hereditary hearing loss stands as the most prevalent sensory disorder, with over 124 non-syndromic genes and approximately 400 syndromic forms of deafness identified in humans. The clinical presentation of these conditions spans a spectrum, ranging from mild to profound hearing loss. The aim of this study was to identify the genetic cause of hearing loss in a family and functionally validate a novel variant identified in the <i>MYO</i>6 gene. After Whole Exome Sequencing analysis, the variant c.2775G>C p.Arg925Ser in <i>MYO</i>6 was detected in a family with postlingual non-syndromic hearing loss. By protein modeling a change in the electrostatic charge of the single alpha helix domain surface was revealed. Through a knockdown phenotype rescue assay in zebrafish, the detrimental effects of the identified variant on the auditory system was determined. These findings underscore the significance of a comprehensive approach, integrating both <i>in silico</i> and <i>in vivo</i> strategies, to ascertain the pathogenicity of this candidate variant. Such an approach has demonstrated its effectiveness in achieving an accurate genetic diagnosis and in promoting a more profound comprehension of the mechanisms that underlie the pathophysiology of hearing.</p>","PeriodicalId":33994,"journal":{"name":"NAR Genomics and Bioinformatics","volume":"6 4","pages":"lqae162"},"PeriodicalIF":4.0000,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632615/pdf/","citationCount":"0","resultStr":"{\"title\":\"<i>In silico</i> and <i>in vivo</i> analyses of a novel variant in <i>MYO</i>6 identified in a family with postlingual non-syndromic hearing loss from Argentina.\",\"authors\":\"Paula I Buonfiglio, Carlos D Bruque, Lucía Salatino, Vanesa Lotersztein, Mariela Pace, Sofia Grinberg, Ana B Elgoyhen, Paola V Plazas, Viviana Dalamón\",\"doi\":\"10.1093/nargab/lqae162\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Hereditary hearing loss stands as the most prevalent sensory disorder, with over 124 non-syndromic genes and approximately 400 syndromic forms of deafness identified in humans. The clinical presentation of these conditions spans a spectrum, ranging from mild to profound hearing loss. The aim of this study was to identify the genetic cause of hearing loss in a family and functionally validate a novel variant identified in the <i>MYO</i>6 gene. After Whole Exome Sequencing analysis, the variant c.2775G>C p.Arg925Ser in <i>MYO</i>6 was detected in a family with postlingual non-syndromic hearing loss. By protein modeling a change in the electrostatic charge of the single alpha helix domain surface was revealed. Through a knockdown phenotype rescue assay in zebrafish, the detrimental effects of the identified variant on the auditory system was determined. These findings underscore the significance of a comprehensive approach, integrating both <i>in silico</i> and <i>in vivo</i> strategies, to ascertain the pathogenicity of this candidate variant. Such an approach has demonstrated its effectiveness in achieving an accurate genetic diagnosis and in promoting a more profound comprehension of the mechanisms that underlie the pathophysiology of hearing.</p>\",\"PeriodicalId\":33994,\"journal\":{\"name\":\"NAR Genomics and Bioinformatics\",\"volume\":\"6 4\",\"pages\":\"lqae162\"},\"PeriodicalIF\":4.0000,\"publicationDate\":\"2024-12-11\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632615/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"NAR Genomics and Bioinformatics\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1093/nargab/lqae162\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/12/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q1\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"NAR Genomics and Bioinformatics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/nargab/lqae162","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/12/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
In silico and in vivo analyses of a novel variant in MYO6 identified in a family with postlingual non-syndromic hearing loss from Argentina.
Hereditary hearing loss stands as the most prevalent sensory disorder, with over 124 non-syndromic genes and approximately 400 syndromic forms of deafness identified in humans. The clinical presentation of these conditions spans a spectrum, ranging from mild to profound hearing loss. The aim of this study was to identify the genetic cause of hearing loss in a family and functionally validate a novel variant identified in the MYO6 gene. After Whole Exome Sequencing analysis, the variant c.2775G>C p.Arg925Ser in MYO6 was detected in a family with postlingual non-syndromic hearing loss. By protein modeling a change in the electrostatic charge of the single alpha helix domain surface was revealed. Through a knockdown phenotype rescue assay in zebrafish, the detrimental effects of the identified variant on the auditory system was determined. These findings underscore the significance of a comprehensive approach, integrating both in silico and in vivo strategies, to ascertain the pathogenicity of this candidate variant. Such an approach has demonstrated its effectiveness in achieving an accurate genetic diagnosis and in promoting a more profound comprehension of the mechanisms that underlie the pathophysiology of hearing.