ArticleDevelopmental biology2015
A critical role for the chromatin remodeller CHD7 in anterior mesoderm during cardiovascular development.
Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Unveiling the Prevalence and Surgical Burden of Neurocristopathies: A Scoping Review and Statistical Analysis.Research square · 2026Article
- Multi-omic analyses identify molecular targets of Chd7 that contribute to CHARGE syndrome model phenotypes.Disease models & mechanisms · 2026Article
- CHD7 regulates cardiac neural crest cell differentiation through SOX5-mediated self-activation.iScience · 2025Article
- CHD7 regulates craniofacial cartilage development via controlling HTR2B expression.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- CHARGE syndrome-associated CHD7 acts at ISL1-regulated enhancers to modulate second heart field gene expression.Cardiovascular research · 2023Article
- ATM-dependent phosphorylation of CHD7 regulates morphogenesis-coupled DSB stress response in fetal radiation exposure.Molecular biology of the cell · 2023Article
- Characterization of Two MouseInternational journal of molecular sciences · 2022Article
- CHD Chromatin Remodeling Protein Diversification Yields Novel Clades and Domains Absent in Classic Model Organisms.Genome biology and evolution · 2022Article
- Chromatin remodeller CHD7 is required for GABAergic neuron development by promoting PAQR3 expression.EMBO reports · 2021Article
- Cardiac Neural Crest Cells: Their Rhombomeric Specification, Migration, and Association with Heart and Great Vessel Anomalies.Cellular and molecular neurobiology · 2021Review
- Cardiac Neural Crest.Cold Spring Harbor perspectives in biology · 2021Review
- Semaphorin Regulation by the Chromatin Remodeler CHD7: An Emerging Genetic Interaction Shaping Neural Cells and Neural Crest in Development and Cancer.Frontiers in cell and developmental biology · 2021Review
- Importance of endothelial Hey1 expression for thoracic great vessel development and its distal enhancer for Notch-dependent endothelial transcription.The Journal of biological chemistry · 2020Article
- CHD7 regulates cardiovascular development through ATP-dependent and -independent activities.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Congenital heart defects in CHARGE: The molecular role of CHD7 and effects on cardiac phenotype and clinical outcomes.American journal of medical genetics. Part C, Seminars in medical genetics · 2020Review
- ATP-Dependent Chromatin Remodeling Complex in the Lineage Specification of Mesenchymal Stem Cells.Stem cells international · 2020Review
- Precision medicine validation: identifying theJournal of feline medicine and surgery · 2019Article
- Sema3E is required for migration of cranial neural crest cells in zebrafish: Implications for the pathogenesis of CHARGE syndrome.International journal of experimental pathology · 2019Article
- Slit-Robo signalling in heart development.Cardiovascular research · 2018Review
- The ATP-dependent chromatin remodeling enzymes CHD6, CHD7, and CHD8 exhibit distinct nucleosome binding and remodeling activities.The Journal of biological chemistry · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
CHARGE syndrome is caused by spontaneous loss-of-function mutations to the ATP-dependant chromatin remodeller chromodomain-helicase-DNA-binding protein 7 (CHD7). It is characterised by a distinct pattern of congenital anomalies, including cardiovascular malformations. Disruption to the neural crest lineage has previously been emphasised in the aetiology of this developmental disorder. We present evidence for an additional requirement for CHD7 activity in the Mesp1-expressing anterior mesoderm during heart development. Conditional ablation of Chd7 in this lineage results in major structural cardiovascular defects akin to those seen in CHARGE patients, as well as a striking loss of cardiac innervation and embryonic lethality. Genome-wide transcriptional analysis identified aberrant expression of key components of the Class 3 Semaphorin and Slit-Robo signalling pathways in Chd7(fl/fl);Mesp1-Cre mutant hearts. CHD7 localises at the Sema3c promoter in vivo, with alteration of the local chromatin structure seen following Chd7 ablation, suggestive of direct transcriptional regulation. Furthermore, we uncover a novel role for CHD7 activity upstream of critical calcium handling genes, and demonstrate an associated functional defect in the ability of cardiomyocytes to undergo excitation-contraction coupling. This work therefore reveals the importance of CHD7 in the cardiogenic mesoderm for multiple processes during cardiovascular development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.