Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN 55905, USA.
J Am Soc Nephrol. 2012 May;23(5):915-33. doi: 10.1681/ASN.2011101032. Epub 2012 Mar 1.
Mutations in two large multi-exon genes, PKD1 and PKD2, cause autosomal dominant polycystic kidney disease (ADPKD). The duplication of PKD1 exons 1-32 as six pseudogenes on chromosome 16, the high level of allelic heterogeneity, and the cost of Sanger sequencing complicate mutation analysis, which can aid diagnostics of ADPKD. We developed and validated a strategy to analyze both the PKD1 and PKD2 genes using next-generation sequencing by pooling long-range PCR amplicons and multiplexing bar-coded libraries. We used this approach to characterize a cohort of 230 patients with ADPKD. This process detected definitely and likely pathogenic variants in 115 (63%) of 183 patients with typical ADPKD. In addition, we identified atypical mutations, a gene conversion, and one missed mutation resulting from allele dropout, and we characterized the pattern of deep intronic variation for both genes. In summary, this strategy involving next-generation sequencing is a model for future genetic characterization of large ADPKD populations.
两个大型多外显子基因 PKD1 和 PKD2 的突变导致常染色体显性多囊肾病 (ADPKD)。PKD1 外显子 1-32 的重复作为 16 号染色体上的六个假基因,等位基因异质性水平高,以及 Sanger 测序的成本使得突变分析复杂化,这有助于 ADPKD 的诊断。我们开发并验证了一种使用下一代测序通过汇集长距离 PCR 扩增子和多重条形码文库来分析 PKD1 和 PKD2 基因的策略。我们使用这种方法对 230 名 ADPKD 患者进行了特征描述。该过程在 183 名典型 ADPKD 患者中的 115 名(63%)中确定了明确的和可能的致病性变体。此外,我们还鉴定了非典型突变、基因转换和一个由于等位基因缺失导致的遗漏突变,并对两个基因的深内含子变异模式进行了特征描述。总之,这种涉及下一代测序的策略是对大型 ADPKD 人群进行遗传特征描述的未来模型。