ArticleNature communications2021
Single cell multi-omic analysis identifies a Tbx1-dependent multilineage primed population in murine cardiopharyngeal mesoderm.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- Reduced dosage of Kmt2d modifies Tbx1 haploinsufficiency toward phenotypes of 22q11.2DS.JCI insight · 2026Article
- Decoding Cardiac Development and Maturation at Single-Cell and Spatial Transcriptomic Resolution.Circulation research · 2026Review
- Integrated multiomics profiling of amniotic fluid exosomes reveals dysregulated lipid and protein signatures in fetal 22q11.2 deletion syndrome.Human genomics · 2026Article
- Neural signaling contributes to heart formation and growth in the invertebrate chordate, Ciona robusta.PLoS biology · 2026Article
- Understanding normal cardiac morphogenesis and its disruptions: a journey through pathways.Frontiers in genetics · 2026Review
- Functional architecture of cardiac TF regulatory landscapes in control of mammalian heart development.bioRxiv : the preprint server for biology · 2025Article
- Cell cycle-driven transcriptome maturation confers multilineage competence to cardiopharyngeal progenitors.The EMBO journal · 2025Article
- Osr1 orchestrates posterior second heart field cell migration for outflow tract formation.Communications biology · 2025Article
- In Vivo Models of Cardiovascular Disease:Biomedicines · 2025Review
- The pericardium forms as a distinct structure during heart formation.Nature communications · 2025Article
- Serine synthesis pathway regulates cardiac differentiation from human pluripotent stem cells.iScience · 2025Article
- A spatiotemporal cell atlas of cardiopulmonary progenitor cell allocation during development.Cell reports · 2025Article
- Mesodermal fibronectin controls cell shape, polarity, and mechanotransduction in the second heart field during cardiac outflow tract development.Developmental cell · 2025Article
- The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024Review
- Gastruloids are competent to specify both cardiac and skeletal muscle lineages.Nature communications · 2024Article
- Single-cell morphometrics reveals T-box gene-dependent patterns of epithelial tension in the Second Heart field.Nature communications · 2024Article
- Multiple embryonic sources converge to form the pectoral girdle skeleton in zebrafish.Nature communications · 2024Article
- Buffering Mechanism in Aortic Arch Artery Formation and Congenital Heart Disease.Circulation research · 2024Article
- Endothelial gene regulatory elements associated with cardiopharyngeal lineage differentiation.Communications biology · 2024Article
- A genome-wide CRISPR screen identifies BRD4 as a regulator of cardiomyocyte differentiation.Nature cardiovascular research · 2024Article
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Authors and funding
17 authors at 7 institutions in 4 countries.
Funding
Abstract
The poles of the heart and branchiomeric muscles of the face and neck are formed from the cardiopharyngeal mesoderm within the pharyngeal apparatus. They are disrupted in patients with 22q11.2 deletion syndrome, due to haploinsufficiency of TBX1, encoding a T-box transcription factor. Here, using single cell RNA-sequencing, we now identify a multilineage primed population within the cardiopharyngeal mesoderm, marked by Tbx1, which has bipotent properties to form cardiac and branchiomeric muscle cells. The multilineage primed cells are localized within the nascent mesoderm of the caudal lateral pharyngeal apparatus and provide a continuous source of cardiopharyngeal mesoderm progenitors. Tbx1 regulates the maturation of multilineage primed progenitor cells to cardiopharyngeal mesoderm derivatives while restricting ectopic non-mesodermal gene expression. We further show that TBX1 confers this balance of gene expression by direct and indirect regulation of enriched genes in multilineage primed progenitors and downstream pathways, partly through altering chromatin accessibility, the perturbation of which can lead to congenital defects in individuals with 22q11.2 deletion syndrome.
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