Suppr超能文献

叉头框蛋白 L1(FOXL1)中的致病缺失鉴定出第一个耳硬化症(OTSC)基因。

A pathogenic deletion in Forkhead Box L1 (FOXL1) identifies the first otosclerosis (OTSC) gene.

机构信息

Faculty of Medicine, Memorial University, St. John's, NL, Canada.

Faculty of Health Sciences, National Centre for Audiology and School of Communication Sciences and Disorders, Western University, London, ON, Canada.

出版信息

Hum Genet. 2022 Apr;141(3-4):965-979. doi: 10.1007/s00439-021-02381-1. Epub 2021 Oct 11.

Abstract

Otosclerosis is a bone disorder of the otic capsule and common form of late-onset hearing impairment. Considered a complex disease, little is known about its pathogenesis. Over the past 20 years, ten autosomal dominant loci (OTSC1-10) have been mapped but no genes identified. Herein, we map a new OTSC locus to a 9.96 Mb region within the FOX gene cluster on 16q24.1 and identify a 15 bp coding deletion in Forkhead Box L1 co-segregating with otosclerosis in a Caucasian family. Pre-operative phenotype ranges from moderate to severe hearing loss to profound sensorineural loss requiring a cochlear implant. Mutant FOXL1 is both transcribed and translated and correctly locates to the cell nucleus. However, the deletion of 5 residues in the C-terminus of mutant FOXL1 causes a complete loss of transcriptional activity due to loss of secondary (alpha helix) structure. FOXL1 (rs764026385) was identified in a second unrelated case on a shared background. We conclude that FOXL1 (rs764026385) is pathogenic and causes autosomal dominant otosclerosis and propose a key inhibitory role for wildtype Foxl1 in bone remodelling in the otic capsule. New insights into the molecular pathology of otosclerosis from this study provide molecular targets for non-invasive therapeutic interventions.

摘要

耳硬化症是一种耳囊骨疾病,也是一种常见的迟发性听力障碍。被认为是一种复杂的疾病,人们对其发病机制知之甚少。在过去的 20 年中,已经确定了十个常染色体显性遗传位点(OTSC1-10),但尚未发现相关基因。在此,我们将一个新的 OTSC 位点定位到 16q24.1 上的 FOX 基因簇内的 9.96 Mb 区域,并在一个白种人家系中发现了一个与耳硬化症共分离的 Forkhead Box L1 编码缺失 15 个碱基对。术前表型范围从中度至重度听力损失到需要植入人工耳蜗的严重感觉神经性听力损失。突变的 FOXL1 既转录又翻译,并正确定位到细胞核。然而,突变 FOXL1 中 C 末端的 5 个残基缺失导致二级(α螺旋)结构缺失,完全丧失转录活性。在另一个具有共同背景的无关病例中也发现了 FOXL1(rs764026385)。我们得出结论,FOXL1(rs764026385)是致病的,导致常染色体显性遗传的耳硬化症,并提出野生型 Foxl1 在耳囊中骨重塑中起关键抑制作用的假说。本研究为耳硬化症的分子病理学提供了新的见解,为非侵入性治疗干预提供了分子靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bc6/9034980/e959df409bb6/439_2021_2381_Fig1_HTML.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验