Nelis E, Timmerman V, De Jonghe P, Muylle L, Martin J J, Van Broeckhoven C
Laboratory of Neurogenetics, Born Bunge Foundation (BBS), University of Antwerp, Belgium.
J Med Genet. 1994 Oct;31(10):811-5. doi: 10.1136/jmg.31.10.811.
Charcot-Marie-Tooth disease type 1 (CMT1) or hereditary motor and sensory neuropathy type I (HMSNI) is an autosomal dominant peripheral neuropathy. In most families the disease segregates with a 1.5 Mb duplication on chromosome 17p11.2 (CMT1A). A few patients have been found with point mutations in the PMP-22 gene. In some families linkage has been found with markers located on chromosome 1q21-q25 (CMT1B) and more recently mutations have been identified in the P0 gene. We analysed an extended CMT1 pedigree (CMT-B) without the CMT1A duplication. Significant positive linkage with chromosome 1 indicated that this family is of the CMT1B subtype. Sequencing of the candidate gene P0 located in chromosome band 1q21-q23 showed a C to A point mutation at position 446 in exon 3 resulting in an Asp134Glu substitution. Since the P0 mutation cosegregated with CMT1 disease we suggest that this mutation is the primary genetic cause of CMT1B in family CMT-B.
1型腓骨肌萎缩症(CMT1)或遗传性运动和感觉性神经病I型(HMSNI)是一种常染色体显性周围神经病。在大多数家族中,该疾病与17号染色体p11.2处1.5 Mb的重复片段(CMT1A)共分离。已发现少数患者的PMP - 22基因存在点突变。在一些家族中,发现与位于1号染色体q21 - q25上的标记存在连锁关系(CMT1B),最近在P0基因中也鉴定出了突变。我们分析了一个没有CMT1A重复片段的CMT1扩展家系(CMT - B)。与1号染色体显著的正连锁表明该家族属于CMT1B亚型。对位于1号染色体带q21 - q23的候选基因P0进行测序,结果显示外显子3中第446位发生了C到A的点突变,导致天冬氨酸134被谷氨酸替代。由于P0突变与CMT1疾病共分离,我们认为该突变是CMT - B家族中CMT1B的主要遗传病因。