A novel cardiomyopathy phenotype linked to a CHD7 missense variant

Abstract Loss of function in the chromatin remodeler CHD7 causes CHARGE syndrome, characterized by variable penetrance and diverse abnormalities. However, establishing genotype-phenotype correlations has been challenging, as most CHD7 inactivating mutations are null alleles. Through CHD7 missense va...

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Main Authors: In Young Park, Chih-Wei Hsu, Karim Bouazoune, Christina E. Espindola, Madeline Hannah McLaughlin Armond, Cristian Coarfa, Sandra L. Grimm, James F. Martin, Donna M. Martin, Cheryl Lyn Walker
Format: Article
Language:English
Published: Nature Portfolio 2025-06-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-00606-1
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author In Young Park
Chih-Wei Hsu
Karim Bouazoune
Christina E. Espindola
Madeline Hannah McLaughlin Armond
Cristian Coarfa
Sandra L. Grimm
James F. Martin
Donna M. Martin
Cheryl Lyn Walker
author_facet In Young Park
Chih-Wei Hsu
Karim Bouazoune
Christina E. Espindola
Madeline Hannah McLaughlin Armond
Cristian Coarfa
Sandra L. Grimm
James F. Martin
Donna M. Martin
Cheryl Lyn Walker
author_sort In Young Park
collection DOAJ
description Abstract Loss of function in the chromatin remodeler CHD7 causes CHARGE syndrome, characterized by variable penetrance and diverse abnormalities. However, establishing genotype-phenotype correlations has been challenging, as most CHD7 inactivating mutations are null alleles. Through CHD7 missense variant analysis at potential phosphorylation sites, we identified T730 (T720 in mice) as a critical residue associated with pathogenesis. Using a CHD7 T730 missense variant (Chd7 T720A) and a frameshift null allele (Chd7 fs) in a mouse model, we found that Chd7 fs/fs mice were non-viable, while Chd7 fs/+ mice exhibited haploinsufficiency-related circling behavior. Notably, Chd7 fs/T720A mice died before postnatal day 2, indicating the Chd7 T720A allele is hypomorphic. Micro-CT analysis at E18.5 revealed that heterozygous mice primarily exhibited hypertrophic cardiomyopathy (HCM), while homozygous mice developed both HCM and dilated cardiomyopathy (DCM). RNA-seq analysis of neonatal Chd7 T720A/T720A hearts revealed a disrupted transcriptome, which in males and females was characterized by downregulation of mitochondrial energy metabolism genes and enrichment of ETS family transcription factor targets. We further identified GSK3β, GSK3α, HIPK1, and DYRK2 as candidate kinases for this site, suggesting a regulatory role in CHD7. This missense variant causing developmental heart abnormalities establishes the first genotype-phenotype correlation for CHD7, and offers new insights into CHARGE syndrome pathogenesis.
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spelling doaj-art-cd98beec3cbf41c5b21f6ccaade7f8222025-08-20T03:10:35ZengNature PortfolioScientific Reports2045-23222025-06-0115111610.1038/s41598-025-00606-1A novel cardiomyopathy phenotype linked to a CHD7 missense variantIn Young Park0Chih-Wei Hsu1Karim Bouazoune2Christina E. Espindola3Madeline Hannah McLaughlin Armond4Cristian Coarfa5Sandra L. Grimm6James F. Martin7Donna M. Martin8Cheryl Lyn Walker9Center for Precision Environmental Health, Baylor College of MedicineDepartment of Integrative Physiology, Baylor College of MedicineCenter for Precision Environmental Health, Baylor College of MedicineCenter for Precision Environmental Health, Baylor College of MedicineCenter for Precision Environmental Health, Baylor College of MedicineDepartment of Duncan Cancer Center-Biostatistics, Baylor College of MedicineDepartment of Duncan Cancer Center-Biostatistics, Baylor College of MedicineDepartment of Integrative Physiology, Baylor College of MedicineDepartment of Pediatrics, University of Michigan Medical SchoolCenter for Precision Environmental Health, Baylor College of MedicineAbstract Loss of function in the chromatin remodeler CHD7 causes CHARGE syndrome, characterized by variable penetrance and diverse abnormalities. However, establishing genotype-phenotype correlations has been challenging, as most CHD7 inactivating mutations are null alleles. Through CHD7 missense variant analysis at potential phosphorylation sites, we identified T730 (T720 in mice) as a critical residue associated with pathogenesis. Using a CHD7 T730 missense variant (Chd7 T720A) and a frameshift null allele (Chd7 fs) in a mouse model, we found that Chd7 fs/fs mice were non-viable, while Chd7 fs/+ mice exhibited haploinsufficiency-related circling behavior. Notably, Chd7 fs/T720A mice died before postnatal day 2, indicating the Chd7 T720A allele is hypomorphic. Micro-CT analysis at E18.5 revealed that heterozygous mice primarily exhibited hypertrophic cardiomyopathy (HCM), while homozygous mice developed both HCM and dilated cardiomyopathy (DCM). RNA-seq analysis of neonatal Chd7 T720A/T720A hearts revealed a disrupted transcriptome, which in males and females was characterized by downregulation of mitochondrial energy metabolism genes and enrichment of ETS family transcription factor targets. We further identified GSK3β, GSK3α, HIPK1, and DYRK2 as candidate kinases for this site, suggesting a regulatory role in CHD7. This missense variant causing developmental heart abnormalities establishes the first genotype-phenotype correlation for CHD7, and offers new insights into CHARGE syndrome pathogenesis.https://doi.org/10.1038/s41598-025-00606-1CHARGE syndromeCHD7T730 phosphorylationCardiomyopathyGSK3
spellingShingle In Young Park
Chih-Wei Hsu
Karim Bouazoune
Christina E. Espindola
Madeline Hannah McLaughlin Armond
Cristian Coarfa
Sandra L. Grimm
James F. Martin
Donna M. Martin
Cheryl Lyn Walker
A novel cardiomyopathy phenotype linked to a CHD7 missense variant
Scientific Reports
CHARGE syndrome
CHD7
T730 phosphorylation
Cardiomyopathy
GSK3
title A novel cardiomyopathy phenotype linked to a CHD7 missense variant
title_full A novel cardiomyopathy phenotype linked to a CHD7 missense variant
title_fullStr A novel cardiomyopathy phenotype linked to a CHD7 missense variant
title_full_unstemmed A novel cardiomyopathy phenotype linked to a CHD7 missense variant
title_short A novel cardiomyopathy phenotype linked to a CHD7 missense variant
title_sort novel cardiomyopathy phenotype linked to a chd7 missense variant
topic CHARGE syndrome
CHD7
T730 phosphorylation
Cardiomyopathy
GSK3
url https://doi.org/10.1038/s41598-025-00606-1
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