Bespalova I N, Adkins S, Pranzatelli M, Burmeister M
Mental Health Research Institute, Department of Human Genetics, University of Michigan, Ann Arbor 48109-0720, USA.
Am J Med Genet. 1997 Sep 19;74(5):467-71. doi: 10.1002/(sici)1096-8628(19970919)74:5<467::aid-ajmg1>3.0.co;2-l.
Two mutations in the cystatin B gene, a 3' splice mutation and a stop codon mutation, were previously found in patients with progressive myoclonus epilepsy of Unverricht-Lundborg type [Pennacchio et al. (1996): Science 271:1731-1734]. We present here a new mutation 2404deltaTC: a 2-bp deletion within the third exon of the cystatin B gene in an Unverricht-Lundborg patient. This mutation results in a frameshift and consequently premature termination of protein synthesis. Complete sequencing of the coding region and splice junctions of the cystatin B gene showed that neither of the two previously known mutations was present in this patient. The level of cystatin B mRNA in an immortalized cell line was found to be decreased, as had been reported for other Unverricht-Lundborg patients. The new mutation further supports the argument that defects in the cystatin B gene cause the Unverricht-Lundborg form of progressive myoclonus epilepsy. We describe a simple PCR method which can detect the 2404deltaTC deletion. This assay, together with previously described PCR assays for the other two known mutations, should prove useful in confirming clinically difficult diagnoses of Unverricht-Lundborg disease.
先前在患有翁韦里希特-伦德伯格型进行性肌阵挛癫痫的患者中发现了胱抑素B基因的两种突变,一种是3'剪接突变,另一种是终止密码子突变[佩纳基奥等人(1996年):《科学》271:1731 - 1734]。我们在此报告一种新的突变2404deltaTC:一名翁韦里希特-伦德伯格患者的胱抑素B基因第三外显子内的2个碱基对缺失。这种突变导致移码,从而导致蛋白质合成提前终止。对胱抑素B基因的编码区和剪接连接进行的全序列分析表明,该患者不存在先前已知的两种突变中的任何一种。正如其他翁韦里希特-伦德伯格患者所报道的那样,在一个永生化细胞系中发现胱抑素B mRNA水平降低。这种新的突变进一步支持了胱抑素B基因缺陷导致翁韦里希特-伦德伯格型进行性肌阵挛癫痫的观点。我们描述了一种能检测2404deltaTC缺失的简单PCR方法。该检测方法与先前描述的针对其他两种已知突变的PCR检测方法一起,在确诊临床上难以诊断的翁韦里希特-伦德伯格病方面应会很有用。