ArticleDevelopment (Cambridge, England)2022
Embryonic requirements for Tcf12 in the development of the mouse coronal suture.
Article in Development (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Clinical and molecular characterization of TCF12 variants in an Asian pediatric cohort with craniosynostosis.BMC medical genomics · 2026Article
- The Transcription Factor 12 of Basic Helix-Loop-Helix Plays an Essential Role in Retinal Health.Investigative ophthalmology & visual science · 2026Article
- Inhibition of craniosynostosis and premature suture fusion inScience advances · 2025Article
- Cellular transitions during cranial suture establishment in zebrafish.Nature communications · 2024Article
- Periostin/Bone Morphogenetic Protein 1 axis axis regulates proliferation and osteogenic differentiation of sutured mesenchymal stem cells and affects coronal suture closure in the TWIST1Journal of orthopaedic surgery and research · 2024Article
- Case report: An adolescent female with anosmic hypogonadotropic hypogonadism, intellectual disability, and papillary thyroid carcinoma: heterozygous deletion ofFrontiers in endocrinology · 2024Article
- Lineage-specific mutation ofFrontiers in physiology · 2023Article
- FGF signaling in cranial suture development and related diseases.Frontiers in cell and developmental biology · 2023Review
- Cranium growth, patterning and homeostasis.Development (Cambridge, England) · 2022Article
- The clinical manifestations, molecular mechanisms and treatment of craniosynostosis.Disease models & mechanisms · 2022Review
- The developing mouse coronal suture at single-cell resolution.Nature communications · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
A major feature of Saethre-Chotzen syndrome is coronal craniosynostosis, the fusion of the frontal and parietal bones at the coronal suture. It is caused by heterozygous loss-of-function mutations in either of the bHLH transcription factors TWIST1 and TCF12. Although compound heterozygous Tcf12; Twist1 mice display severe coronal synostosis, the individual role of Tcf12 had remained unexplored. Here, we show that Tcf12 controls several key processes in calvarial development, including the rate of frontal and parietal bone growth, and the boundary between sutural and osteogenic cells. Genetic analysis supports an embryonic requirement for Tcf12 in suture formation, as combined deletion of Tcf12 in embryonic neural crest and mesoderm, but not in postnatal suture mesenchyme, disrupts the coronal suture. We also detected asymmetric distribution of mesenchymal cells on opposing sides of the wild-type frontal and parietal bones, which prefigures later bone overlap at the sutures. In Tcf12 mutants, reduced asymmetry is associated with bones meeting end-on-end, possibly contributing to synostosis. Our results support embryonic requirements of Tcf12 in proper formation of the overlapping coronal suture.
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Registered trials
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.