Wehnert M, Hopwood J J, Schröder W, Herrmann F H
Institut für Medizinische Genetik, Ernst Moritz Arndt-Universität, Greifswald, Federal Republic of Germany.
Hum Genet. 1992 Jun;89(4):430-2. doi: 10.1007/BF00194316.
A total of 14 unrelated German patients with X-linked iduronate-2-sulfatase (IDS) deficiency (Hunter syndrome, MPS II) showing variable clinical manifestations was screened for structural gene aberrations by Southern analysis. Using the IDS cDNA clone c2S15 as a probe, no Southern fragments could be detected in blots in the severely affected patient G-65 with respect to DNA digested by HindIII, PstI and TaqI, suggesting a total loss of the IDS structural gene. In this patient, the flanking loci DXS 297, DXS 296 and DXS 466 were tested. The locus DXS 466 is involved in the deletion, whereas both of the other loci are present. A normal 9.0-kb fragment disappeared and an aberrant fragment of 3.5 kb occurred in the HindIII blot of patient G-117. A normal Southern pattern was found in PstI and TaqI blots of this patient. This result can be interpreted as the generation of an additional HindIII restriction site by point mutation in an IDS gene intron.
通过Southern印迹分析,对14例临床表现各异的、患有X连锁艾杜糖醛酸-2-硫酸酯酶(IDS)缺乏症(亨特综合征,黏多糖贮积症II型)的非亲缘关系德国患者进行了结构基因畸变筛查。使用IDS cDNA克隆c2S15作为探针,在严重受累患者G - 65中,相对于经HindIII、PstI和TaqI消化的DNA,在印迹中未检测到Southern片段,提示IDS结构基因完全缺失。在该患者中,对侧翼基因座DXS 297、DXS 296和DXS 466进行了检测。基因座DXS 466参与了缺失,而其他两个基因座均存在。在患者G - 117的HindIII印迹中,一个正常的9.0 kb片段消失,出现了一个3.5 kb的异常片段。在该患者的PstI和TaqI印迹中发现了正常的Southern模式。这一结果可解释为IDS基因内含子中的点突变产生了一个额外的HindIII限制性酶切位点。