Recessive genetic contribution to congenital heart disease in 5,424 probands

W Weilai Dong (Department of Genetics, Yale School of Medicine) S Sheng Chih Jin M Michael C. Sierant (Department of Genetics, Yale School of Medicine) Z Ziyu Lu B Boyang Li (Department of Mechanical Engineering and Materials Science) Q Qiongshi Lu (Department of Biostatistics and Medical Informatics, University of Wisconsin) S Sarah U. Morton (Division of Newborn Medicine, Department of Pediatrics, Boston Children’s Hospital) J Junhui Zhang F Francesc Lopez-Giraldez C Carol Nelson-Williams (Department of Genetics, Yale School of Medicine) J James R. Knight (Yale Center for Genome Analysis, Yale University) H Hongyu Zhao J Junyue Cao S Shrikant Mane P Peter J. Gruber (Department of Surgery, Yale University School of Medicine) M Monkol Lek (Department of Genetics, Yale School of Medicine) E Elizabeth Goldmuntz (Division of Cardiology, Children’s Hospital of Philadelphia, Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania) J John Deanfield (Institute of Cardiovascular Science, University College London) A Alessandro Giardini (Pediatric Cardiology, Great Ormond Street Hospital) S Seema Mital M Mark Russell (Department of Pediatrics and Communicable Diseases, University of Michigan) J J. William Gaynor (Division of Cardiothoracic Surgery, Children's Hospital of Philadelphia) J James F. Cnota (Division of Cardiology, Cincinnati Children’s Hospital Medical Center) M Michael Wagner D Deepak Srivastava D Daniel Bernstein (Department of Pediatrics, Cardiology, Stanford University) G George A. Porter (Department of Pediatrics, Section of Cardiology, Yale School of Medicine) J Jane Newburger (Department of Cardiology, Boston Children’s Hospital) A Amy E. Roberts (Department of Cardiology, Boston Children’s Hospital, Harvard Medical School) M Mark Yandell (Department of Human Genetics, University of Utah and School of Medicine) H H. Joseph Yost (Department of Human Genetics, University of Utah and School of Medicine) M Martin Tristani-Firouzi (Division of Pediatric Cardiology, University of Utah) R Richard Kim (Pediatric Cardiac Surgery, Smidt Heart Institute, Cedars-Sinai Medical Center) J Jonathan Seidman (Department of Genetics, Harvard Medical School) W Wendy K. Chung (Department of Pediatrics, Boston Children’s Hospital, Harvard Medical School) B Bruce D. Gelb (Mindich Child Health and Development Institute, Icahn School of Medicine at Mount Sinai) C Christine E. Seidman R Richard P. Lifton (Laboratory of Human Genetics and Genomics, The Rockefeller University) M Martina Brueckner (Department of Genetics, Yale School of Medicine)

Abstract

Variants with large effect contribute to congenital heart disease (CHD). To date, recessive genotypes (RGs) have commonly been implicated through anecdotal ascertainment of consanguineous families and candidate gene-based analysis; the recessive contribution to the broad range of CHD phenotypes has been limited. We analyzed whole exome sequences of 5,424 CHD probands. Rare damaging RGs were estimated to contribute to at least 2.2% of CHD, with greater enrichment among laterality phenotypes (5.4%) versus other subsets (1.4%). Among 108 curated human recessive CHD genes, there were 66 RGs, with 54 in 11 genes with >1 RG, 12 genes with 1 RG, and 85 genes with zero. RGs were more prevalent among offspring of consanguineous union (4.7%, 32/675) than among nonconsanguineous probands (0.7%, 34/4749). Founder variants in GDF1 and PLD1 accounted for 74% of the contribution of RGs among 410 Ashkenazi Jewish probands. We identified genome-wide significant enrichment of RGs in C1orf127 , encoding a likely secreted protein expressed in embryonic mouse notochord and associated with laterality defects. Single-cell transcriptomes from gastrulation-stage mouse embryos revealed enrichment of RGs in genes highly expressed in the cardiomyocyte lineage, including contractility-related genes MYH6, UNC45B , MYO18B , and MYBPC3 in probands with left-sided CHD, consistent with abnormal contractile function contributing to these malformations. Genes with significant RG burden account for 1.3% of probands, more than half the inferred total. These results reveal the recessive contribution to CHD, and indicate that many genes remain to be discovered, with each likely accounting for a very small fraction of the total.

Article Details

Volume / Issue Vol. 122, Issue 10
Published March 11, 2025
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (39)

W

Weilai Dong

Department of Genetics, Yale School of Medicine

S

Sheng Chih Jin

M

Michael C. Sierant

Department of Genetics, Yale School of Medicine

Z

Ziyu Lu

B

Boyang Li

Department of Mechanical Engineering and Materials Science

Q

Qiongshi Lu

Department of Biostatistics and Medical Informatics, University of Wisconsin

S

Sarah U. Morton

Division of Newborn Medicine, Department of Pediatrics, Boston Children’s Hospital

J

Junhui Zhang

F

Francesc Lopez-Giraldez

C

Carol Nelson-Williams

Department of Genetics, Yale School of Medicine

J

James R. Knight

Yale Center for Genome Analysis, Yale University

H

Hongyu Zhao

J

Junyue Cao

S

Shrikant Mane

P

Peter J. Gruber

Department of Surgery, Yale University School of Medicine

M

Monkol Lek

Department of Genetics, Yale School of Medicine

E

Elizabeth Goldmuntz

Division of Cardiology, Children’s Hospital of Philadelphia, Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania

J

John Deanfield

Institute of Cardiovascular Science, University College London

A

Alessandro Giardini

Pediatric Cardiology, Great Ormond Street Hospital

S

Seema Mital

M

Mark Russell

Department of Pediatrics and Communicable Diseases, University of Michigan

J

J. William Gaynor

Division of Cardiothoracic Surgery, Children's Hospital of Philadelphia

J

James F. Cnota

Division of Cardiology, Cincinnati Children’s Hospital Medical Center

M

Michael Wagner

D

Deepak Srivastava

D

Daniel Bernstein

Department of Pediatrics, Cardiology, Stanford University

G

George A. Porter

Department of Pediatrics, Section of Cardiology, Yale School of Medicine

J

Jane Newburger

Department of Cardiology, Boston Children’s Hospital

A

Amy E. Roberts

Department of Cardiology, Boston Children’s Hospital, Harvard Medical School

M

Mark Yandell

Department of Human Genetics, University of Utah and School of Medicine

H

H. Joseph Yost

Department of Human Genetics, University of Utah and School of Medicine

M

Martin Tristani-Firouzi

Division of Pediatric Cardiology, University of Utah

R

Richard Kim

Pediatric Cardiac Surgery, Smidt Heart Institute, Cedars-Sinai Medical Center

J

Jonathan Seidman

Department of Genetics, Harvard Medical School

W

Wendy K. Chung

Department of Pediatrics, Boston Children’s Hospital, Harvard Medical School

B

Bruce D. Gelb

Mindich Child Health and Development Institute, Icahn School of Medicine at Mount Sinai

C

Christine E. Seidman

R

Richard P. Lifton

Laboratory of Human Genetics and Genomics, The Rockefeller University

M

Martina Brueckner

Department of Genetics, Yale School of Medicine