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NIPBL rearrangements in Cornelia de Lange syndrome: evidence for replicative mechanism and genotype-phenotype correlation
Journal article   Open access   Peer reviewed

NIPBL rearrangements in Cornelia de Lange syndrome: evidence for replicative mechanism and genotype-phenotype correlation

Davut Pehlivan, Melanie Hullings, Claudia M. B. Carvalho, Claudia G. Gonzaga-Jauregui, Elizabeth Loy, Laird G. Jackson, Ian D. Krantz, Matthew A. Deardorff and James R. Lupski
Genetics in medicine, v 14(3), pp 313-322
01 Mar 2012
PMID: 22241092
url
https://www.nature.com/articles/gim201113.pdfView
Published, Version of Record (VoR) Open

Abstract

Genetics & Heredity Life Sciences & Biomedicine Science & Technology
Purpose: Cornelia de Lange syndrome (CdLS) is a multisystem congenital anomaly disorder characterized by mental retardation, limb abnormalities, distinctive facial features, and hirsutism. Mutations in three genes involved in sister chromatid cohesion, NIPBL, SMC1A, and SMC3, account for similar to 55% of CdLS cases. The molecular etiology of a significant fraction of CdLS cases remains unknown. We hypothesized that large genomic rearrangements of cohesin complex subunit genes may play a role in the molecular etiology of this disorder. Methods: Custom high-resolution oligonucleotide array comparative genomic hybridization analyses interrogating candidate cohesin genes and breakpoint junction sequencing of identified genomic variants were performed. Results: Of the 162 patients with CdLS, for whom mutations in known CdLS genes were previously negative by sequencing, deletions containing NIPBL exons were observed in 7 subjects (similar to 5%). Breakpoint sequences in five patients implicated microhomology-mediated replicative mechanisms such as serial replication slippage and fork stalling and template switching/microhomology-mediated break-induced replication as a potential predominant contributor to these copy number variations. Most deletions are predicted to result in haploinsufficiency due to heterozygous loss-of-function mutations; such mutations may result in a more severe CdLS phenotype. Conclusion: Our findings suggest a potential clinical utility to testing for copy number variations involving NIPBL when clinically diagnosed CdLS cases are mutation-negative by DNA-sequencing studies.

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Genetics & Heredity
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