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扩展由致病性 ARSG 变异引起的 Usher 综合征 IV 型的遗传图谱。

Expanding the genetic landscape of Usher syndrome type IV caused by pathogenic ARSG variants.

机构信息

Center for Medical Genetics, Ghent University Hospital & Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.

Department of Ophthalmology, University Hospital Leuven, Leuven, Belgium.

出版信息

Clin Genet. 2025 Jan;107(1):44-55. doi: 10.1111/cge.14614. Epub 2024 Aug 28.

Abstract

Usher syndrome (USH) is the most common cause of deafblindness. USH is autosomal recessively inherited and characterized by rod-cone dystrophy or retinitis pigmentosa (RP), often accompanied by sensorineural hearing loss. Variants in >15 genes have been identified as causative for clinically and genetically distinct subtypes. Among the ultra-rare and recently discovered genes is ARSG, coding for the lysosomal sulfatase Arylsulfatase G. This subtype was assigned as "USH IV" with a late onset of RP and usually late-onset progressive SNHL without vestibular involvement. Here, we describe nine new subjects and the clinical description of four cases with the USH IV phenotype bearing seven novel and two known pathogenic variants. Functional experiments indicated the complete loss of sulfatase enzymatic activity upon ectopic expression of mutated ARSG cDNA. Interestingly, we identified a homozygous missense variant, p.(Arg99His), previously described in dogs with neuronal ceroid lipofuscinosis. Our study expands the genetic landscape of ARSG-USH IV and the number of known subjects by more than 30%. These findings highlight that USH IV likely has been underdiagnosed and emphasize the need to test molecularly unresolved subjects with deafblindness syndrome. Finally, testing of ARSG should be considered for the genetic work-up of apparent isolated inherited retinal diseases.

摘要

Usher 综合征(USH)是最常见的聋盲症病因。USH 为常染色体隐性遗传,特征为视杆-视锥营养不良或视网膜色素变性(RP),常伴有感觉神经性听力损失。>15 个基因的变异已被确定为具有临床和遗传上明显不同亚型的致病原因。在最近发现的超罕见基因中,有 ARSG,编码溶酶体硫酸酯酶 Arylsulfatase G。这种亚型被指定为“USH IV”,具有 RP 的晚发性发病和通常无前庭受累的晚发性进行性 SNHL。在这里,我们描述了 9 名新患者,并介绍了 4 名具有 USH IV 表型的患者的临床描述,他们携带 7 种新的和 2 种已知的致病性变异。功能实验表明,突变 ARSG cDNA 的异位表达完全丧失了硫酸酯酶的酶活性。有趣的是,我们发现了一种纯合错义变异,p.(Arg99His),之前在患有神经元蜡样脂褐质沉积症的狗中描述过。我们的研究扩展了 ARSG-USH IV 的遗传图谱,使已知的患者数量增加了 30%以上。这些发现表明,USH IV 可能一直被误诊,并强调需要对聋盲综合征的分子未解决患者进行检测。最后,对于表现为孤立遗传性视网膜疾病的患者,应考虑进行 ARSG 的检测。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbd6/11608847/ad9fa82d2916/CGE-107-44-g005.jpg

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