Yokota I, Indo Y, Coates P M, Tanaka K
Department of Human Genetics, Yale University School of Medicine, New Haven, Connecticut 06510.
J Clin Invest. 1990 Sep;86(3):1000-3. doi: 10.1172/JCI114761.
We sequenced polymerase chain reaction (PCR)-amplified variant medium chain acyl-CoA dehydrogenase (MCAD) cDNAs in cultured fibroblasts from three MCAD-deficient patients. In all three patients, an A to G transition was identified at position 985 of the coding region. Since no appropriate restriction sites for detecting this point mutation were found, we devised a PCR method that amplifies an 87-bp fragment from position 955. In the 5' primer encompassing positions 955 to 984, A-981 was artificially substituted with C. With the presence of C-981 and G-985, an Nco I restriction site is introduced in the mutant copies. When cDNA or genomic DNA from fibroblasts of nine MCAD-deficient patients were tested with this method, the copies from all of them completely cleaved into two shorter fragments by Nco I, indicating their homozygosity for the A----G-985 transition. In contrast, the copies from all eight controls remained intact. Thus, this A----G-985 transition is the single prevalent mutation causing MCAD deficiency, a highly unusual feature for any genetic disorder. The PCR/Nco I digestion method is suitable for the diagnosis of MCAD deficiency.
我们对来自三名中链酰基辅酶A脱氢酶(MCAD)缺乏症患者的培养成纤维细胞中的聚合酶链反应(PCR)扩增的变异MCAD互补DNA(cDNA)进行了测序。在所有三名患者中,在编码区第985位发现了A到G的转换。由于未找到用于检测此点突变的合适限制性酶切位点,我们设计了一种PCR方法,该方法从第955位扩增出一个87碱基对的片段。在包含第955至984位的5'引物中,A-981被人为替换为C。由于存在C-981和G-985,在突变体拷贝中引入了一个Nco I限制性酶切位点。当用此方法检测来自九名MCAD缺乏症患者成纤维细胞的cDNA或基因组DNA时,所有样本的拷贝都被Nco I完全切割成两个较短的片段,表明它们在A----G-985转换上是纯合的。相比之下,所有八个对照样本的拷贝都保持完整。因此,这种A----G-985转换是导致MCAD缺乏症的单一常见突变,这对于任何遗传疾病来说都是非常不寻常的特征。PCR/Nco I消化方法适用于MCAD缺乏症的诊断。