Sukegawa K, Tomatsu S, Fukao T, Iwata H, Song X Q, Yamada Y, Fukuda S, Isogai K, Orii T
Department of Pediatrics, Gifu University School of Medicine, Japan.
Hum Mutat. 1995;6(2):136-43. doi: 10.1002/humu.1380060206.
Mucopolysaccharidosis type II (Hunter disease) is a lysosomal storage disorder caused by a deficiency of the enzyme iduronate-2-sulfatase. Varied clinical phenotypes of this disease have been described. To identify mutations in individual patients and to examine possible correlations between mutations and clinical phenotypes, we analyzed the iduronate-2-sulfatase gene in Japanese patients with different clinical phenotypes. Five missense mutations, S333L (severe), R468Q (severe), R468L (severe), W337R (intermediate), R48P (mild), and three nonsense mutations, W345X (severe), R443X (intermediate), Q531X (mild), were identified by the RT-PCR method. Transient expression in the enzyme-deficient fibroblasts revealed that all five missense mutant enzymes were synthesized as the normal-size precursor (73 kD), and the nonsense mutant enzymes were synthesized as truncated ones (W345X:54 kD, R443X:59 kD, and Q531X:69 kD), although stable mature enzymes (45-56 kD) were not detected by Western blot analysis. Furthermore, expression of the eight mutant cDNAs resulted in severe reductions of iduronate-2-sulfatase enzyme activity in comparison with a normal cDNA.
II型粘多糖贮积症(亨特病)是一种溶酶体贮积病,由艾杜糖醛酸-2-硫酸酯酶缺乏引起。已描述了该疾病的多种临床表型。为了鉴定个体患者中的突变,并研究突变与临床表型之间可能的相关性,我们分析了不同临床表型的日本患者的艾杜糖醛酸-2-硫酸酯酶基因。通过RT-PCR方法鉴定出5个错义突变,即S333L(重度)、R468Q(重度)、R468L(重度)、W337R(中度)、R48P(轻度),以及3个无义突变,即W345X(重度)、R443X(中度)、Q531X(轻度)。在酶缺陷的成纤维细胞中瞬时表达显示,所有5个错义突变酶均作为正常大小的前体(73 kD)合成,无义突变酶则作为截短的酶合成(W345X:54 kD、R443X:59 kD和Q531X:69 kD),尽管通过蛋白质印迹分析未检测到稳定的成熟酶(45 - 56 kD)。此外,与正常cDNA相比,8个突变cDNA的表达导致艾杜糖醛酸-2-硫酸酯酶活性严重降低。