Carstens Nadia, Williams Susan, Goolam Saadiah, Carmichael Trevor, Cheung Ming Sin, Büchmann-Møller Stine, Sultan Marc, Staedtler Frank, Zou Chao, Swart Peter, Rice Dennis S, Lacoste Arnaud, Paes Kim, Ramsay Michèle
Sydney Brenner Institute for Molecular Bioscience, University of the Witwatersrand, 2050, Johannesburg, Gauteng, South Africa.
Division of Ophthalmology, Department of Neurosciences, University of the Witwatersrand, Johannesburg, South Africa.
BMC Med Genet. 2016 Jul 20;17(1):47. doi: 10.1186/s12881-016-0308-0.
Macular corneal dystrophy (MCD) is a rare autosomal recessive disorder that is characterized by progressive corneal opacity that starts in early childhood and ultimately progresses to blindness in early adulthood. The aim of this study was to identify the cause of MCD in a black South African family with two affected sisters.
A multigenerational South African Sotho-speaking family with type I MCD was studied using whole exome sequencing. Variant filtering to identify the MCD-causal mutation included the disease inheritance pattern, variant minor allele frequency and potential functional impact.
Ophthalmologic evaluation of the cases revealed a typical MCD phenotype and none of the other family members were affected. An average of 127 713 variants per individual was identified following exome sequencing and approximately 1.2 % were not present in any of the investigated public databases. Variant filtering identified a homozygous E71Q mutation in CHST6, a known MCD-causing gene encoding corneal N-acetyl glucosamine-6-O-sulfotransferase. This E71Q mutation results in a non-conservative amino acid change in a highly conserved functional domain of the human CHST6 that is essential for enzyme activity.
We identified a novel E71Q mutation in CHST6 as the MCD-causal mutation in a black South African family with type I MCD. This is the first description of MCD in a black Sub-Saharan African family and therefore contributes valuable insights into the genetic aetiology of this disease, while improving genetic counselling for this and potentially other MCD families.
黄斑角膜营养不良(MCD)是一种罕见的常染色体隐性疾病,其特征是角膜逐渐混浊,始于儿童早期,最终在成年早期发展为失明。本研究的目的是确定一个有两名患病姐妹的南非黑人家庭中MCD的病因。
使用全外显子组测序研究了一个讲南非索托语的多代I型MCD家族。用于识别MCD致病突变的变异筛选包括疾病遗传模式、变异小等位基因频率和潜在功能影响。
对病例的眼科评估显示出典型的MCD表型,且其他家庭成员均未受影响。外显子组测序后,每个个体平均鉴定出127713个变异,其中约1.2%在任何被调查的公共数据库中均未出现。变异筛选在CHST6中鉴定出一个纯合的E71Q突变,CHST6是一个已知的导致MCD的基因,编码角膜N-乙酰葡糖胺-6-O-磺基转移酶。这种E71Q突变导致人CHST6高度保守的功能域中发生非保守氨基酸变化,而该功能域对酶活性至关重要。
我们在一个患有I型MCD的南非黑人家庭中鉴定出CHST6基因中的一种新型E71Q突变作为MCD致病突变。这是撒哈拉以南非洲黑人家庭中MCD的首次描述,因此为该疾病的遗传病因提供了有价值的见解,同时改善了对这个以及其他可能的MCD家庭的遗传咨询。