Contribution of rare inherited and de novo variants in 2,871 congenital heart disease probands.

TitleContribution of rare inherited and de novo variants in 2,871 congenital heart disease probands.
Publication TypeJournal Article
Year of Publication2017
AuthorsJin, SChih, Homsy, J, Zaidi, S, Lu, Q, Morton, S, DePalma, SR, Zeng, X, Qi, H, Chang, W, Sierant, MC, Hung, W-C, Haider, S, Zhang, J, Knight, J, Bjornson, RD, Castaldi, C, Tikhonoa, IR, Bilguvar, K, Mane, SM, Sanders, SJ, Mital, S, Russell, MW, J Gaynor, W, Deanfield, J, Giardini, A, Porter, GA, Srivastava, D, Lo, CW, Shen, Y, W Watkins, S, Yandell, M, H Yost, J, Tristani-Firouzi, M, Newburger, JW, Roberts, AE, Kim, R, Zhao, H, Kaltman, JR, Goldmuntz, E, Chung, WK, Seidman, JG, Gelb, BD, Seidman, CE, Lifton, RP, Brueckner, M
JournalNat Genet
Volume49
Issue11
Pagination1593-1601
Date Published2017 Nov
ISSN1546-1718
KeywordsAdult, Autistic Disorder, Cardiac Myosins, Case-Control Studies, Child, Exome, Female, Gene Expression, Genetic Predisposition to Disease, Genome-Wide Association Study, Growth Differentiation Factor 1, Heart Defects, Congenital, Heterozygote, High-Throughput Nucleotide Sequencing, Homozygote, Humans, Male, Mutation, Myosin Heavy Chains, Pedigree, Risk, Vascular Endothelial Growth Factor Receptor-3
Abstract

Congenital heart disease (CHD) is the leading cause of mortality from birth defects. Here, exome sequencing of a single cohort of 2,871 CHD probands, including 2,645 parent-offspring trios, implicated rare inherited mutations in 1.8%, including a recessive founder mutation in GDF1 accounting for ∼5% of severe CHD in Ashkenazim, recessive genotypes in MYH6 accounting for ∼11% of Shone complex, and dominant FLT4 mutations accounting for 2.3% of Tetralogy of Fallot. De novo mutations (DNMs) accounted for 8% of cases, including ∼3% of isolated CHD patients and ∼28% with both neurodevelopmental and extra-cardiac congenital anomalies. Seven genes surpassed thresholds for genome-wide significance, and 12 genes not previously implicated in CHD had >70% probability of being disease related. DNMs in ∼440 genes were inferred to contribute to CHD. Striking overlap between genes with damaging DNMs in probands with CHD and autism was also found.

DOI10.1038/ng.3970
Alternate JournalNat. Genet.
PubMed ID28991257
PubMed Central IDPMC5675000
Grant ListU01 HL098163 / HL / NHLBI NIH HHS / United States
UM1 HL098162 / HL / NHLBI NIH HHS / United States
UM1 HL098123 / HL / NHLBI NIH HHS / United States
UL1 TR001863 / TR / NCATS NIH HHS / United States
U01 HL098188 / HL / NHLBI NIH HHS / United States
U01 HL098162 / HL / NHLBI NIH HHS / United States
S10 OD018521 / OD / NIH HHS / United States
U01 HL098153 / HL / NHLBI NIH HHS / United States
U01 HL131003 / HL / NHLBI NIH HHS / United States
S10 OD018522 / OD / NIH HHS / United States
U54 HG006504 / HG / NHGRI NIH HHS / United States
U01 HL098180 / HL / NHLBI NIH HHS / United States
UL1 TR000003 / TR / NCATS NIH HHS / United States
UM1 HL098160 / HL / NHLBI NIH HHS / United States
R01 GM104390 / GM / NIGMS NIH HHS / United States
R01 HL132024 / HL / NHLBI NIH HHS / United States
T32 GM007205 / GM / NIGMS NIH HHS / United States
U01 HL098160 / HL / NHLBI NIH HHS / United States
U01 HL098123 / HL / NHLBI NIH HHS / United States
U54 HD090255 / HD / NICHD NIH HHS / United States
UM1 HL128711 / HL / NHLBI NIH HHS / United States
UM1 HL098147 / HL / NHLBI NIH HHS / United States
U01 HL098147 / HL / NHLBI NIH HHS / United States