Steglich C, Bunge S, Hulsebos T, Beck M, Brandt N J, Schwinger E, Hopwood J J, Gal A
Institut für Humangenetik der Medizinischen Universität, Lübeck, Germany.
Hum Genet. 1993 Sep;92(2):179-82. doi: 10.1007/BF00219688.
Hunter disease is an X-linked mucopolysaccharidosis caused by deficiency of the lysosomal enzyme iduronate-2-sulfatase (IDS). Using the IDS cDNA and DNA probes corresponding to loci flanking the IDS locus, we performed molecular genetic studies in two patients with Hunter syndrome. An interstitial deletion spanning the middle part of the IDS gene was found in the first patient. The second patient carries a gross gene rearrangement that can be detected after HindIII or EcoRI digestion of genomic DNA, and is similar to that found recently in seven unrelated Hunter patients. Our data suggest that the structural aberration observed is a partial intragenic inversion. As the same altered hybridization pattern is also revealed by the recently described anonymous DNA probe II-10, which recognizes a frequent TaqI restriction fragment length polymorphism at the DXS466 locus, we conclude that DXS466 maps within the IDS gene, probably in an intron.
亨特氏病是一种由溶酶体酶艾杜糖醛酸-2-硫酸酯酶(IDS)缺乏引起的X连锁黏多糖贮积症。我们使用IDS cDNA以及与IDS基因座侧翼位点相对应的DNA探针,对两名亨特综合征患者进行了分子遗传学研究。在第一名患者中发现了一个跨越IDS基因中部的间质缺失。第二名患者携带一种明显的基因重排,在基因组DNA经HindIII或EcoRI酶切后即可检测到,且与最近在七名无关的亨特氏病患者中发现的情况相似。我们的数据表明,观察到的结构畸变是部分基因内倒位。由于最近描述的匿名DNA探针II-10也揭示了相同的改变后的杂交模式,该探针识别DXS466基因座处常见的TaqI限制性片段长度多态性,我们得出结论,DXS466定位于IDS基因内,可能在内含子中。