Allanson J E, Gemmill R M, Hecht B K, Johnsen S, Wenger D A
Genetics Center, Southwest Biomedical Research Institute, Scottsdale, AZ 85251.
Am J Med Genet. 1988 Mar;29(3):517-22. doi: 10.1002/ajmg.1320290307.
GUSB, the gene for beta-glucuronidase, has been localized to the proximal long arm of chromosome 7 between 7q11.2 and 7q22. Deficiency of beta-glucuronidase results in mucopolysaccharidosis type VII (MPS VII, Sly syndrome). The enzymatic defect has been demonstrated in cultured skin fibroblasts, leukocytes and serum of affected patients. An 8-yr-old boy presented with manifestations similar to MPS VII (mental retardation, short stature, "coarse" facial appearance, mild skeletal involvement and recurrent lower respiratory tract infection) but other, discrepant abnormalities, e.g., bilateral iris colobomata and cleft palate. Normal activity of beta-glucuronidase was found in the patient's leukocytes. Chromosome analysis disclosed an interstitial deletion of 7q with one breakpoint at the interface between bands 11.22 and 11.23 and the other breakpoint within band 21.1. DNA from this patient's leukocytes was analyzed for dosage of GUSB sequences. This locus appeared to be present at the normal diploid level. These findings suggest that GUSB is not in the portion of chromosome 7 deleted in our case, narrowing the smallest region of overlap to 7q21.1----7q22. We therefore assign the beta-glucuronidase gene to 7q21.1----7q22.
β-葡萄糖醛酸酶基因(GUSB)已被定位于7号染色体长臂近端,在7q11.2和7q22之间。β-葡萄糖醛酸酶缺乏会导致黏多糖贮积症VII型(MPS VII,斯利综合征)。在受影响患者的培养皮肤成纤维细胞、白细胞和血清中已证实存在酶缺陷。一名8岁男孩表现出与MPS VII相似的症状(智力发育迟缓、身材矮小、面容“粗糙”、轻度骨骼受累和反复下呼吸道感染),但还有其他不一致的异常情况,如双侧虹膜缺损和腭裂。在该患者的白细胞中发现β-葡萄糖醛酸酶活性正常。染色体分析显示7q存在间质性缺失,一个断点位于11.22和11.23带之间的界面处,另一个断点在21.1带内。对该患者白细胞的DNA进行了GUSB序列剂量分析。该基因座似乎以正常二倍体水平存在。这些发现表明,在我们的病例中,GUSB不在7号染色体缺失的部分,将最小重叠区域缩小到7q21.1----7q22。因此,我们将β-葡萄糖醛酸酶基因定位于7q21.1----7q22。