| Literature DB >> 22383692 |
Sandro Rossetti1, Katharina Hopp, Robert A Sikkink, Jamie L Sundsbak, Yean Kit Lee, Vickie Kubly, Bruce W Eckloff, Christopher J Ward, Christopher G Winearls, Vicente E Torres, Peter C Harris.
Abstract
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.Entities:
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Year: 2012 PMID: 22383692 PMCID: PMC3338301 DOI: 10.1681/ASN.2011101032
Source DB: PubMed Journal: J Am Soc Nephrol ISSN: 1046-6673 Impact factor: 10.121