| Literature DB >> 32662247 |
Jihai Xu1, Jing Wu2, Xiaofeng Teng1, Libing Cai1, Huizong Yuan1, Xiaokun Chen3, Mu Hu4, Xin Wang1, Ning Jiang5, Hong Chen1.
Abstract
Polydactyly and syndactyly are digital abnormalities in limb-associated birth defects usually caused by genetic disorders. In this study, a five-generation Chinese pedigree was found with triphalangeal thumb polysyndactyly syndrome (TPTPS), showing an autosomal dominant pattern of inheritance. We utilized linkage analysis and whole genome sequencing (WGS) for the genetic diagnosis of this pedigree. Linkage analysis was performed using a genome-wide single nucleotide polymorphism (SNP) chip and three genomic regions were identified in chromosomes 2, 6, and 7 with significant linkage signals. WGS discovered a copy number variation (CNV) mutation caused by a large duplication region at the tail of chromosome 7 located in exons 1-5 of the LMBR1 gene, including the zone of polarizing activity regulatory sequence (ZRS), with a length of approximately 180 kb. A real-time polymerase chain reaction (PCR) assay confirmed the duplication. The findings of our study supported the notion that large duplications including the ZRS caused TPTPS. Our study showed that linkage analysis in combination with WGS could successfully identify the disease locus and causative mutation in TPTPS, which could help elucidate the molecular mechanisms and genotype-phenotype correlations in polydactyly.Entities:
Keywords: LMBR1; copy number variations; linkage analysis; polydactyly; whole genome sequencing
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Year: 2020 PMID: 32662247 DOI: 10.1002/ajmg.a.61757
Source DB: PubMed Journal: Am J Med Genet A ISSN: 1552-4825 Impact factor: 2.802