Correction: Genome-Wide Copy Number Analysis Uncovers a New HSCR Gene: NRG3

Clara Sze-Man Tang(Harvard University), Guo Cheng(Chinese University of Hong Kong), Man‐Ting So(Chinese University of Hong Kong), Benjamin Hon Kei Yip(Harvard University), Xiaoping Miao(Chinese University of Hong Kong), Emily Hoi-Man Wong(Chinese University of Hong Kong), Esw Ngan(Chinese University of Hong Kong), Vincent Chi‐Hang Lui(Chinese University of Hong Kong), You‐Qiang Song(Chinese University of Hong Kong), Danny Chan(Chinese University of Hong Kong), Kmc Cheung(Chinese University of Hong Kong), Zhenwei Yuan(China Medical University), Lei Liu(Shenzhen Children's Hospital), Bhy Chung(Chinese University of Hong Kong), Xuelai Liu(Chinese University of Hong Kong), Kenneth Kak‐Yuen Wong(Harvard University), Christian R. Marshall(Chinese University of Hong Kong), Stephen W. Scherer(University of Toronto), Stacey S. Cherny(Chinese University of Hong Kong), Pak-Chung Sham(Chinese University of Hong Kong), Paul Kwong‐Hang Tam(Chinese University of Hong Kong), Maria-Mercà ̈ Garcia-BarcelÃ
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Abstract

Hirschsprung disease (HSCR) is a congenital disorder characterized by aganglionosis of the distal intestine. To assess the contribution of copy number variants (CNVs) to HSCR, we analysed the data generated from our previous genome-wide association study on HSCR patients, whereby we identified NRG1 as a new HSCR susceptibility locus. Analysis of 129 Chinese patients and 331 ethnically matched controls showed that HSCR patients have a greater burden of rare CNVs (p = 1.50610 25 ), particularly for those encompassing genes (p = 5.00610 26 ). Our study identified 246 rare-genic CNVs exclusive to patients. Among those, we detected a NRG3 deletion (p = 1.64610 23 ). Subsequent follow-up (96 additional patients and 220 controls) on NRG3 revealed 9 deletions (combined p = 3.36610 25 ) and 2 de novo duplications among patients and two deletions among controls. Importantly, NRG3 is a paralog of NRG1. Stratification of patients by presence/ absence of HSCR-associated syndromes showed that while syndromic-HSCR patients carried significantly longer CNVs than the non-syndromic or controls (p = 1.50610 25 ), non-syndromic patients were enriched in CNV number when compared to controls (p = 4.00610 26 ) or the syndromic counterpart. Our results suggest a role for NRG3 in HSCR etiology and provide insights into the relative contribution of structural variants in both syndromic and non-syndromic HSCR. This would be the first genome-wide catalog of copy number variants identified in HSCR.


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