Mok Andrea, Cao Henian, Hegele Robert A
Robarts Research Institute, London, Ontario, Canada N6A 5K8.
Genomics. 2003 Jan;81(1):1-5. doi: 10.1016/s0888-7543(02)00014-9.
Mucopolysaccharidosis type IIID (MPS IIID; Sanfilippo syndrome type D; MIM 252940) is caused by deficiency of the activity of N-acetylglucosamine-6-sulfatase (GNS), which is normally required for degradation of heparan sulfate. The clinical features of MPS IIID include progressive neurodegeneration, with relatively mild somatic symptoms. Biochemical features include accumulation of heparan sulfate and N-acetylglucosamine-6-sulfate in the brain and viscera. To date, diagnosis required a specific lysosomal enzyme assay for GNS activity. From genomic DNA of a subject with MPS IIID, we amplified and sequenced the promoter and 14 exons of GNS. We found a homozygous nonsense mutation in exon 9 (1063C --> T), which predicted premature termination of translation (R355X). We also identified two common synonymous coding single-nucleotide polymorphisms and genotyped these in samples from four ethnic groups. This first report of a mutation in GNS resulting in MPS IIID indicates the potential utility of molecular diagnosis for this rare condition.
IIID型黏多糖贮积症(MPS IIID;D型Sanfilippo综合征;MIM 252940)是由N-乙酰葡糖胺-6-硫酸酯酶(GNS)活性缺乏引起的,该酶是硫酸乙酰肝素降解所必需的。MPS IIID的临床特征包括进行性神经退行性变,伴有相对较轻的躯体症状。生化特征包括脑和内脏中硫酸乙酰肝素和N-乙酰葡糖胺-6-硫酸盐的蓄积。迄今为止,诊断需要对GNS活性进行特定的溶酶体酶测定。从一名MPS IIID患者的基因组DNA中,我们扩增并测序了GNS的启动子和14个外显子。我们在第9外显子中发现了一个纯合的无义突变(1063C→T),这预测了翻译的提前终止(R355X)。我们还鉴定了两个常见的同义编码单核苷酸多态性,并在来自四个种族群体的样本中对其进行了基因分型。这篇关于导致MPS IIID的GNS突变的首次报道表明了分子诊断对这种罕见疾病的潜在效用。