Birot A M, Bouton O, Froissart R, Maire I, Bozon D
Laboratoire de Biochimie Pédiatrique, Hôpital Debrousse, Lyon, France.
Hum Mutat. 1996;8(1):44-50. doi: 10.1002/(SICI)1098-1004(1996)8:1<44::AID-HUMU6>3.0.CO;2-P.
Hunter disease or mucopolysaccharidosis type II is an X-linked disease caused by the deficiency of the lysosomal enzyme iduronate-2-sulfatase (IDS). The IDS gene (24 kb) contains nine exons and has been completely sequenced. A pseudogene (IDS-2 locus) distal to the functional IDS gene has recently been identified. This work reports the characterization of IDS gene alterations in two severely affected patients. Patient 1 has a partial deletion that removes exons I to VI and extends about 200 kb upstream of the IDS gene. Patient 2 has an internal deletion of exons IV, V, VI, and VII, which results from an IDS gene-pseudogene exchange between highly homologous regions. In the rearranged gene, the junction intron contains pseudogene intron 3- and intron 7-related sequences. An interchromosomal recombination is probably the cause of this rearranged X chromosome.
亨特氏病或II型粘多糖贮积症是一种X连锁疾病,由溶酶体酶艾杜糖醛酸-2-硫酸酯酶(IDS)缺乏引起。IDS基因(24 kb)包含9个外显子,并且已完成全序列测定。最近在功能性IDS基因远端发现了一个假基因(IDS-2位点)。这项工作报道了两名重症患者中IDS基因改变的特征。患者1存在部分缺失,缺失外显子I至VI,并延伸至IDS基因上游约200 kb处。患者2存在外显子IV、V、VI和VII的内部缺失,这是由于高度同源区域之间的IDS基因-假基因交换所致。在重排基因中,连接内含子包含假基因内含子3和内含子7相关序列。染色体间重组可能是这条重排X染色体的成因。