Title | Contribution of rare inherited and de novo variants in 2,871 congenital heart disease probands. |
Publication Type | Journal Article |
Year of Publication | 2017 |
Authors | Jin, 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 |
Journal | Nat Genet |
Volume | 49 |
Issue | 11 |
Pagination | 1593-1601 |
Date Published | 2017 Nov |
ISSN | 1546-1718 |
Keywords | Adult, 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. |
DOI | 10.1038/ng.3970 |
Alternate Journal | Nat. Genet. |
PubMed ID | 28991257 |
PubMed Central ID | PMC5675000 |
Grant List | U01 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 |