ArticleDevelopment (Cambridge, England)2025
FGFR2 directs inhibition of WNT signaling to regulate anterior fontanelle closure during skull development.
Article in Development (Cambridge, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Fzd7 Restrains Pink1-Dependent Mitophagy in Suture Stem Cells to Maintain Cranial Suture Patency.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fgfr3-Wnt signaling crosstalk is involved in maintaining cranial suture integrity.Bone research · 2026Article
- ERK-Mediated Phosphorylation of YAP Defines a Noncanonical FGF Signaling Mechanism in Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TGFβ-mediated dural progenitor cell migration into the coronal suture is crucial for preventing craniosynostosis.Nature communications · 2026Article
- TGF-β/BMP signaling in skeletal biology: molecular mechanisms, regulatory networks, and therapeutic implications in development, regeneration, and disease.Bone research · 2026Review
- Further Evidence of Early-Onset Osteoporosis and Bone Fractures as a NewInternational journal of molecular sciences · 2025Article
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Abstract
The calvarial bones of the infant skull are linked by transient fibrous joints known as sutures and fontanelles, which are essential for skull compression during birth and expansion during postnatal brain growth. Genetic conditions caused by pathogenic variants in FGFR2, such as Apert, Pfeiffer, and Crouzon syndromes, result in calvarial deformities due to premature suture fusion and a persistently open anterior fontanelle (AF). In this study, we investigated how Fgfr2 regulates AF closure by leveraging mouse genetics and single-cell transcriptomics. We find that AF cells, marked by the tendon/ligament factor SCX, are spatially organized into ecto- and endocranial domains that selectively differentiate into ligament, bone, and cartilage to form the posterior frontal suture. We show that AF cell differentiation is non-autonomously regulated by FGFR2 signaling in osteogenic front cells of the frontal bones, which regulate WNT signaling in neighboring AF cells by expressing the secreted WNT inhibitor Wif1. Upon loss of Fgfr2, Wif1 expression is downregulated, and AF cells fail to form the posterior frontal suture. This study identifies an FGF-WNT signaling circuit that that directs suture formation within the AF during postnatal development.
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