Laccone F, Huppke P, Hanefeld F, Meins M
Institute of Human Genetics, Georg-August-University Göttingen, Göttingen, Germany.
Hum Mutat. 2001 Mar;17(3):183-90. doi: 10.1002/humu.3.
Mutations in the MECP2 (Methyl-CpG-binding protein) gene recently have been reported to cause Rett syndrome (RTT), an X-linked dominant neurodevelopmental disease. We investigated 125 sporadic cases of Rett syndrome by direct sequencing. Thirty different mutations were found in 97 patients with Rett syndrome. Seventeen mutations have not been described previously. We provide evidence for the existence of several hot spot regions and of a deletion-prone region located at the 3' most region of the gene. This latter region most probably forms secondary structures in vitro. Similar structures in vivo could explain the high frequency of deletions in this region. Nine of 10 recurrent mutations were located in either the methyl CpG binding domain (MBD) or in the transcriptional repression domain (TRD), and all missense mutations were located in one of these functionally important domains. There was a high frequency of more than 60% of truncating mutations (nonsense mutations along with frameshift mutations). One patient with a mild form of the disease and a normal head growth carries a novel c.27-6C>A mutation that causes a cryptic splice site in intron I resulting in a frameshift transcript. The detection rate in our collective was 77.6%. Our findings show that the majority of German Rett patients carry mutations in the MECP2 gene confirming the suggested locus homogeneity for the disease.
最近有报道称,甲基化CpG结合蛋白2(MECP2)基因的突变会导致瑞特综合征(RTT),这是一种X连锁显性神经发育疾病。我们通过直接测序对125例散发性瑞特综合征病例进行了研究。在97例瑞特综合征患者中发现了30种不同的突变。其中17种突变此前未曾被描述过。我们提供了证据,证明该基因存在几个热点区域以及位于基因最3'端的一个易于发生缺失的区域。后一个区域在体外很可能形成二级结构。体内类似的结构可以解释该区域缺失的高频率。10个反复出现的突变中有9个位于甲基化CpG结合结构域(MBD)或转录抑制结构域(TRD),并且所有错义突变都位于这些功能重要的结构域之一。截短突变(无义突变和移码突变)的频率高达60%以上。一名患有轻度疾病且头部生长正常的患者携带一种新的c.27-6C>A突变,该突变导致内含子I中出现一个隐蔽的剪接位点,从而产生移码转录本。我们研究群体中的检测率为77.6%。我们的研究结果表明,大多数德国瑞特患者在MECP2基因中携带突变,证实了该疾病所提示的位点同质性。