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全基因组测序揭示了导致常染色体显性遗传性黄斑变性的新突变。

Whole genome sequencing reveals novel mutations causing autosomal dominant inherited macular degeneration.

作者信息

Borooah Shyamanga, Stanton Chloe M, Marsh Joseph, Carss Keren J, Waseem Naushin, Biswas Pooja, Agorogiannis Georgios, Raymond Lucy, Arno Gavin, Webster Andrew R

机构信息

a Department of Ophthalmology , Moorfields Eye Hospital , London , UK.

b Centre for Clinical Brain Sciences, School of Clinical Sciences , University of Edinburgh , Edinburgh , UK.

出版信息

Ophthalmic Genet. 2018 Dec;39(6):763-770. doi: 10.1080/13816810.2018.1546406. Epub 2018 Nov 19.

Abstract

BACKGROUND

Age-related macular degeneration (AMD) is a common sight threatening condition. However, there are a number of monogenic macular dystrophies that are clinically similar to AMD, which can potentially provide pathogenetic insights.

METHODS

Three siblings from a non-consanguineous Greek-Cypriot family reported central visual disturbance and nyctalopia. The patients had full ophthalmic examinations and color fundus photography, spectral-domain ocular coherence tomography and scanning laser ophthalmoscopy. Targeted polymerase chain reaction (PCR) was performed as a first step to attempt to identify suspected mutations in C1QTNF5 and TIMP3 followed by whole genome sequencing.

RESULTS

The three patients were noted to have symptoms of nyctalopia, early paracentral visual field loss and, in older patients, central vision loss. Imaging identified pseudodrusen, retinal atrophy and RPE-Bruch's membrane separation. Whole genome sequencing of the proband revealed two novel heterozygous variants in C1QTNF5, c.556C>T, and c.569C>G. The mutation segregated with disease in this family, occurred in cis, and resulted in missense amino acid changes P186S and S190W in C1QTNF5. In silico modeling of the variants revealed that the S190W mutations was likely to have the greatest pathologic effect and that the combination of the mutations was likely to have an additive effect.

CONCLUSIONS

The novel mutations in C1QTNF5 identified here expand the genotypic spectrum of mutations causing late-onset retinal dystrophy.

摘要

背景

年龄相关性黄斑变性(AMD)是一种常见的致盲性疾病。然而,有许多单基因黄斑营养不良在临床上与AMD相似,这可能为发病机制提供见解。

方法

一个非近亲的希腊裔塞浦路斯家庭的三名兄弟姐妹报告有中心视力障碍和夜盲症。对患者进行了全面的眼科检查、彩色眼底照相、光谱域光学相干断层扫描和扫描激光检眼镜检查。作为第一步,进行靶向聚合酶链反应(PCR)以尝试鉴定C1QTNF5和TIMP3中的疑似突变,随后进行全基因组测序。

结果

三名患者均有夜盲症症状、早期旁中心视野缺损,老年患者有中心视力丧失。影像学检查发现假性玻璃膜疣、视网膜萎缩和视网膜色素上皮-布鲁赫膜分离。先证者的全基因组测序显示C1QTNF5中有两个新的杂合变异,即c.556C>T和c.569C>G。该突变在这个家族中与疾病共分离,呈顺式发生,并导致C1QTNF5中错义氨基酸改变P186S和S190W。对这些变异的计算机模拟显示,S190W突变可能具有最大的病理效应,且这些突变的组合可能具有累加效应。

结论

此处鉴定出的C1QTNF5新突变扩展了导致迟发性视网膜营养不良的突变基因型谱。

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