Berg T, Riise H M, Hansen G M, Malm D, Tranebjaerg L, Tollersrud O K, Nilssen O
Department of Medical Genetics, University Hospital and University of Tromso, N-9037, Norway.
Am J Hum Genet. 1999 Jan;64(1):77-88. doi: 10.1086/302183.
alpha-Mannosidosis is an autosomal recessive disorder caused by deficiency of lysosomal alpha-mannosidase (LAMAN). The resulting intracellular accumulation of mannose-containing oligosaccharides leads to mental retardation, hearing impairment, skeletal changes, and immunodeficiency. Recently, we reported the first alpha-mannosidosis-causing mutation affecting two Palestinian siblings. In the present study 21 novel mutations and four polymorphic amino acid positions were identified by the screening of 43 patients, from 39 families, mainly of European origin. Disease-causing mutations were identified in 72% of the alleles and included eight splicing, six missense, and three nonsense mutations, as well as two small insertions and two small deletions. In addition, Southern blot analysis indicated rearrangements in some alleles. Most mutations were private or occurred in two or three families, except for a missense mutation resulting in an R750W substitution. This mutation was found in 13 patients, from different European countries, and accounted for 21% of the disease alleles. Although there were clinical variations among the patients, no significant LAMAN activity could be detected in any of the fibroblast cultures. In addition, no correlation between the types of mutations and the clinical manifestations was evident.
α-甘露糖苷贮积症是一种常染色体隐性疾病,由溶酶体α-甘露糖苷酶(LAMAN)缺乏引起。由此导致的含甘露糖寡糖在细胞内蓄积会引发智力迟钝、听力障碍、骨骼变化和免疫缺陷。最近,我们报道了首例影响两名巴勒斯坦同胞的α-甘露糖苷贮积症致病突变。在本研究中,通过对来自39个家庭、主要为欧洲血统的43名患者进行筛查,鉴定出21个新突变和4个多态性氨基酸位点。在72%的等位基因中鉴定出致病突变,包括8个剪接突变、6个错义突变、3个无义突变,以及2个小插入和2个小缺失。此外,Southern印迹分析表明一些等位基因存在重排。除导致R750W替换的错义突变外,大多数突变是个别发生的或出现在两三个家庭中。该突变在来自不同欧洲国家的13名患者中被发现,占疾病等位基因的21%。尽管患者之间存在临床差异,但在任何成纤维细胞培养物中均未检测到显著的LAMAN活性。此外,突变类型与临床表现之间没有明显的相关性。