Rathmann M, Bunge S, Beck M, Kresse H, Tylki-Szymanska A, Gal A
Institut für Humangenetik, Universitäts-Krankenhaus Eppendorf, Hamburg, Germany.
Am J Hum Genet. 1996 Dec;59(6):1202-9.
Mucopolysaccharidosis type II (MPS II, Hunter syndrome) is an X-chromosomal storage disorder due to deficiency of the lysosomal enzyme iduronate-2-sulfatase (IDS). We have identified IDS mutations in a total of 31 families/patients with MPS II, of which 20 are novel and unique and a further 1 is novel but has been found in 3 unrelated patients. One of the mutations detected is of special interest as an AG-->G substitution in an intron, far apart from the coding region, is deleterious by creating a new 5'-splice-donor site that results in the inclusion of a 78-bp intronic sequence. While the distribution of gene rearrangements (deletions, insertions, and duplications) of <20 bp seems to be random over the IDS gene, the analysis of a total of 101 point mutations lying within the coding region shows that they tend to be more frequent in exons III, VIII, and IX. Forty-seven percent of the point mutations are at CpG dinucleotides, of which G:C-to-A:T transitions constitute nearly 80%. Almost all recurrent point mutations involve CpG sites. Analysis of a collective of 50 families studied in our laboratory, to date, revealed that mutations occur more frequently in male meioses (estimated male-to-female ratio between 3.76 and 6.3).
II型黏多糖贮积症(MPS II,亨特综合征)是一种X染色体隐性遗传性溶酶体贮积症,因溶酶体酶艾杜糖醛酸-2-硫酸酯酶(IDS)缺乏所致。我们在总共31个MPS II家庭/患者中鉴定出了IDS突变,其中20个是新的且独特的,另有1个是新的但已在3名无亲缘关系的患者中发现。检测到的其中一个突变特别有趣,因为在内含子中一个远离编码区的AG→G替换是有害的,它产生了一个新的5'-剪接供体位点,导致包含一个78bp的内含子序列。虽然<20bp的基因重排(缺失、插入和重复)在IDS基因上的分布似乎是随机的,但对编码区内总共101个点突变的分析表明,它们在外显子III、VIII和IX中往往更频繁。47%的点突变位于CpG二核苷酸处,其中G:C到A:T的转换占近80%。几乎所有反复出现的点突变都涉及CpG位点。对我们实验室迄今为止研究的50个家庭的汇总分析表明,突变在男性减数分裂中更频繁发生(估计男女比例在3.76至6.3之间)。