Department of Medical Genetics, Eberhard-Karls-University, Tübingen, Germany.
Neurogenetics. 2012 Aug;13(3):215-27. doi: 10.1007/s10048-012-0329-6. Epub 2012 May 3.
Hereditary spastic paraplegias (HSP) are a heterogeneous group of neurological disorders. Insidiously progressive spastic weakness of the lower extremities is the common criterion in all forms described. Clinically, HSP is differentiated into pure (uncomplicated) and complex (complicated) forms. While pure HSP is predominantly characterized by signs and symptoms of pyramidal tract dysfunction, additional neurological and non-neurological symptoms occur in complicated forms. Autosomal dominant, autosomal recessive, and X-linked modes of inheritance have been described and at least 48 subtypes, termed SPG1-48, have been genetically defined. Although in autosomal dominant HSP families 50-60% of etiologies can be established by genetic testing, genotype predictions based on the phenotype are limited. In order to realize high-throughput genotyping for dominant HSP, we designed a resequencing microarray for six autosomal dominant genes on the Affymetrix CustomSEQ array platform. For validation purposes, 10 previously Sanger sequenced patients with autosomal dominant HSP and 40 positive controls with known mutations in ATL1, SPAST, NIPA1, KIF5A, and BSCL2 (32 base exchanges, eight small indels) were resequenced on this array. DNA samples of 45 additional patients with AD spastic paraplegia were included in the study. With two different sequencing analysis software modules (GSEQ, SeqC), all missense/nonsense mutations in the positive controls were identified while indels had a detection rate of only 50%. In total, 244 common synonymous single-nucleotide polymorphisms (SNPs) annotated in dbSNP (build 132) corresponding to 22 distinct sequence variations were found in the 53 analyzed patients. Among the 22 different sequence variations (SPAST n = 15, ATL1 n = 3, KIF5A n = 2, HSPD1 n = 1, BSCL2 n = 1, NIPA1 n = 0), 12 were rare variants that have not been previously described and whose clinical significance is unknown. In SPAST-negative cases, a genetic diagnosis could be established in 11% by resequencing. Resequencing microarray technology can therefore efficiently be used to study genotypes and mutations in large patient cohorts.
遗传性痉挛性截瘫(HSP)是一组异质性的神经疾病。所有描述的形式都以下肢进行性痉挛性无力为共同标准。临床上,HSP 分为单纯(单纯型)和复杂(复杂型)两种形式。单纯 HSP 主要表现为锥体束功能障碍的体征和症状,而复杂型则出现额外的神经和非神经症状。已描述了常染色体显性、常染色体隐性和 X 连锁遗传方式,至少已确定 48 种亚型,称为 SPG1-48。尽管在常染色体显性 HSP 家族中,50-60%的病因可通过基因检测确定,但基于表型的基因型预测是有限的。为了实现显性 HSP 的高通量基因分型,我们在 Affymetrix CustomSEQ 阵列平台上为六个常染色体显性基因设计了一个重测序微阵列。为了验证目的,对 10 名先前通过 Sanger 测序的常染色体显性 HSP 患者和 40 名已知 ATL1、SPAST、NIPA1、KIF5A 和 BSCL2 突变的阳性对照者(32 个碱基交换,8 个小插入缺失)进行了该阵列的重测序。该研究还纳入了 45 名额外的常染色体显性痉挛性截瘫患者的 DNA 样本。使用两种不同的测序分析软件模块(GSEQ、SeqC),在阳性对照中均能识别所有错义/无义突变,而插入缺失的检测率仅为 50%。总共在 53 名分析患者中发现了 244 个常见同义单核苷酸多态性(SNP),这些 SNP 在 dbSNP(构建号 132)中被注释,对应 22 个不同的序列变异。在 22 个不同的序列变异(SPAST n = 15、ATL1 n = 3、KIF5A n = 2、HSPD1 n = 1、BSCL2 n = 1、NIPA1 n = 0)中,有 12 个是以前未描述过的罕见变异,其临床意义尚不清楚。在 SPAST 阴性病例中,通过重测序可确定 11%的遗传诊断。因此,重测序微阵列技术可有效地用于研究大患者队列的基因型和突变。